In the following paper I am going to cover the extensive harms that can be done by vaccination, in particular the reactivation of vaccine viruses,^[1] and the 8 common human herpesviruses (Herpes simplex 1 & 2 (HSV-1, HSV-2), Varicella Zoster Virus (VZV/chickenpox), Epstein-Barr Virus (EBV), Human Cytomegalovirus (HCMV), Human Herpesvirus 6 (HHV-6), Human Herpesvirus 7 (HHV-7), Human Herpesvirus 8 (HHV-8), as well as the contaminant viruses like SV40, JC Virus, and BK Virus that more than half the country inherited by 1960 from contaminated polio vaccines.^[2]

I am going to show how both vaccine viruses and the reactivation of latent viruses often triggered by vaccinations are the most likely culprits in the cause of autism, with MMR vaccines being notorious for triggering autism. This is due to reactivation of the vaccine viruses in immunosuppressed children, either experiencing immune deficiencies from past vaccines, stealth infections, or direct immunosuppression from the triple dose of viruses in the MMR vaccine given at a time when their immune systems are hardly developed to fight off the multiple overlapping infections in one vaccine.

What is autism? Our public health officials tell us it is an inherited genetic neurodevelopmental disorder, but after all the research I’ve done studying people like Erich Traub and all of his discoveries this is clearly a poor explanation. The literature shows autistic-spectrum disorder (ASD) to be immune-mediated, which suggests it is para-infectious in origin. One paper clearly shows:

This PRISMA-ScR-guided scoping review synthesizes contemporary evidence to propose a structured immunological classification of ASD comprising six immune-related subtypes: immune overactivation, immune deficiency, autoimmunity-linked ASD, gut-immune axis dysregulation, post-infectious or immune-triggered onset patterns, and maternal immune activation. Each subtype is defined by characteristic neuroimmune features - including cytokine imbalances, aberrant microglial activation, altered microbiome-immune communication, and prenatal immune priming - reflecting distinct biological pathways through which immune dysfunction may influence neurodevelopment.^[3]

That would directly imply immune tolerance pathways. The public health establishment viciously denies the claim that autism is caused by vaccination, saying that it has been thoroughly debunked but the studies they cite to backup this claim are all insufficient and faulty. They utilize clever angles and omissions of the factors surrounding immune tolerance to get the desired results they’re seeking. They claim the autism link is vaccine misinformation, but this paper will point out that more evidence than not suggests that it can indeed be caused or triggered directly by any vaccine suppressing the immune system and reactivating either vaccine viruses or latent neurotropic viruses. The available published scientific literature also explains vaguely how it works if you analyze the right papers and go far enough back in the history of virology, immunology, and vaccinology to study immune tolerance and persistent infections. Erich Traub’s work on immune tolerance, reactivation of latent viruses, persistent infection, and the “slow virus disease,” show us how it works.^[4]

Without understanding these fundamental tenets of immunology and virology in Traub’s work, we are left in the dark. However, once these are understood, we can see the mechanics of how vaccination can cause autism and many other neurological diseases like that cited in older literature discussing “post-vaccinal encephalitis.”^[5]

In the 2000s, it became highly controversial to claim autism and vaccination were linked and Big Pharma set out to crucify and publicly ruin anyone who dared to point out the connection,^[6] because the vaccine industry would have been finished by the new millennium if we had dealt with it honestly and with safety in mind. Regardless of what one thinks of Dr. Andrew Wakefield, it’s neither here nor there because none of my argument depends on any of Wakefield’s work or his original paper involving the gut. I have discovered research fully independent of Wakefield that lends increasing weight to the overall idea that vaccines can and do cause autism.

Personally, I think Wakefield’s approach was complicated from the start because although MMR could be notorious for triggering autistic spectrum disorders in many cases, the literature and the history seems to lend more weight that it can be caused by several para-infectious co-factors interacting, including immunosuppression, vaccination with multiple different vaccines and the reactivation of vaccine viruses and dormant viruses already infecting the child. Stealth co-infections could also play a role.^[7]

It may be true that foreign intelligence services use the vaccine debate as a divisive wedge to divide the American people,^[8] but that doesn’t mean that the harm surrounding vaccines is unfounded. I can assure you the harms are very much there and we’re gambling with our lives every time we take these injections to give us some sense of security by taking an even more dangerous risk. The following information will show numerous contradictions in the official position and their dishonesty will become apparent when you follow the science that has been laid out from the discoveries of Erich Traub onward. It is scattered in the scientific literature across the topics of antigen, neurotropic viruses, and immune tolerance discussed in my book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare.^[9]

Erich Traub’s discoveries reactivating dormant viruses by injecting foreign antigen (simulating a vaccine) show us how many of these chronic diseases work,^[10] due to the induced immune deficiencies later coined “immune tolerance.”^[11] The underlying idea behind immune tolerance is that the body is exhausted and forced to tolerate harmful pathogens it should otherwise be keeping out of the body because it is immunosuppressed^[12] trying to fight off antigen that undergoes constant antigenic variation.^[13] Traub also showed us how neurological wasting diseases followed in its wake,^[14] because it was always a rebound effect of immunodeficiencies following exposure to high concentrations of antigen.^[15] In turn, viruses would reactivate and attack the brain and central nervous system.^[16] For a young child, this would occur during the most critical time of the brain’s development.^[17] It was always part and parcel of the immune tolerance phenomenon which is a modest term for chronic immune deficiency. It is elucidated from para-infectious mechanisms and high exposure to antigens – the main ingredients of the vaccine.

Genes may play a role in the factors surrounding susceptibility to developing autism making some more predisposed than others, but bad genes are not itself the cause. It would be akin to blaming the HLA for an infectious disease. HLA is the genetic predisposition of different immune system types for their susceptibility to certain diseases,^[18] but you would not blame the infection on the genes and say that is caused by bad genes and it is the same with autism. It is rather an immunosuppressive state often but not always presenting with gastrointestinal co-factors but mainly driven by neurotropic viral infections inflaming the brain during the critical years of development. All of the low-grade inflammation seen in autistic spectrum disorders would be missed in MRI scans.^[19] This has been discussed by Karl Bechter in his paper Virus Infection as a Cause of Inflammation in Psychiatric Disorders, and these same blind spots in diagnosis he cites also apply to autistic spectrum disorders and to most any disease caused by reactivation of latent viruses which can be caused by vaccinations of all kinds:

Many neurotropic viruses exist and may cause classical inflammation but also low-level neuroinflammation. However, viruses may be dormant within the CNS and become active later. The role of neurotropic virus infections in the causation of psychiatric disorders may be underestimated, because the diagnostic approach to the CNS is difficult and to dormant infections in general, but especially within the CNS. Evidence is increasing that infections increase the risk of psychiatric disorders, not only prenatal infections but also infections during the lifetime. The question how low level neuroinflammation may be involved in severe psychiatric disorders like affective and schizophrenic spectrum disorders is intriguing but remains to be studied. Experimental data clearly show that low-level neuroinflammation can be induced by viruses, but the definitions of inflammation and low level neuroinflammation appear to be blurred and apparently the previous classical definition of inflammation has to be widened. Virus infection itself or virus-related products or virus-induced autoimmunity may play a role in disease pathogenesis. More sensitive diagnostic approaches from neuroimaging and CSF investigations may hold the key to a better understanding and definition of CNS viral infections as an etiopathogenetic subgroup of severe psychiatric disorders.^[20]

Vaccines are a major cause of the reactivation of latent viruses, and this is a widespread phenomenon published in the scientific literature. But here’s how we know that vaccines, especially MMR, can cause autism. The published science admits that MMR vaccines can cause a fatal progressive infection with the vaccine viruses called Subacute Sclerosing Panencephalitis (SSPE). SSPE is a progressive, fatal persistent measles virus infection which is sometimes a reaction to the vaccine viruses reactivating causing persistent infection and progressively destroying the brain. They show that, in the beginning stages, SSPE looks indistinguishable from autism. This was shown in a 1997 paper Measles, mumps, rubella vaccine induced subacute sclerosing panencephalitis:

This paper reports the case of a 15-year-old girl from India who developed SSPE presumably as a result of a delayed effect of measles, mumps, and rubella (MMR) vaccine. She presented with a 2-month history of behavioral disturbances, a deterioration in school performance, forgetfulness, silly smiling, handwriting changes, social withdrawal, and ataxia. The girl had received MMR vaccine at 9 months of age and had no past history of measles.^[21]

For many fatal diseases, there are also chronic non-fatal forms that would affect the large majority. So naturally, if SSPE can happen from the vaccine on rare occasions, which is the fatal version, there would be a similar chronic non-fatal form that would be far more common, which would look exactly like autism. Instead of becoming a progressive and fatal infection, immunosuppression kicks in and forms a stable parasitism between vaccine virus and the host. It can maintain this equilibrium for a lifetime, but eventually in the future it would turn in favor of the vaccine virus. Erich Traub had noted a similar phenomenon with Equine Infectious Anemia Virus early in World War II.^[22]

In a 1973 paper Neurologic Disorders Following Live Measles-Virus Vaccination, one can find descriptions of such non-fatal adverse events in which extensive long-term neurological diseases followed after being confirmed as being caused by the vaccine. This was long before the topic became politically charged and controversial, where vaccine injured cases were left with learning disabilities (mirroring autism), retardation, and symptoms often found in combination with autism such as ataxia (poor muscle coordination and balance), hyperkinesis (excessive motor activity, restlessness, and impulsivity), and seizures (occur in up to 40% of autistic children):

Group A—All of the remaining 59 patients had extensive neurologic disorders. Five were fatal. Symptoms in all began 1 to 25 days after vaccination, but 45 (76%) had onset on days 6 to 15 (Fig 1), the period when virus replication is maximal, after primary live-virus vaccination, and when viremia is expected to occur. […] Measles virus was isolated on the ninth day after inoculation from the CSF of one patient who had developed ataxia and choreoathetosis seven days after vaccination; preliminary studies of tissue culture sensitivity, plaquing, and infectivity titer indicate this isolate to be of a vaccine-like virus. […] Recent follow-up information or report of death was obtained for 50 (85%) of these 59 patients. Twenty-six (52%) had recovered fully, five (10%) had died, and 19 (38%) were left with neurologic sequelae. Residual neurologic findings included ataxia in 2 patients, retardation in 11, and learning disability or hyperkinesis in another 3, seizure disorders in 9, and hemiparesis in 4.^[23]

Para-infectious mechanisms involved in autism would also explain why autistic children are said to develop bigger brains (megalencephaly) than normal children.^[24] Inflammation from stealth viral infections can certainly play a role in the formation of megalencephaly.^[25] The multiple viruses in the MMR vaccine (mumps, measles, rubella) or other vaccines can suppress the immune system at which point the vaccine viruses or latent herpesviruses (EBV, HHV-6, HCMV, HSV, etc.) reactivate and start inflaming the brain at critical times of development.^[26]

By the basic ideas presented in this article, MMR vaccine could be potentially notorious for triggering autism when immunosuppression is present. Also, many Western children are probably born with congenital infections inherited from their mothers.^[27] This even includes reactivated viruses from vaccines their mothers got before they were conceived or born and then passed to them, mirroring Traub’s LCM Virus studies.^[28] This is exactly what happened in Traub’s LCM Virus experiments,^[29] he reactivated a dormant virus with a vaccine and started an epidemic from scratch and all sick females would invariably give birth to immune tolerant virus-infected mice born without any antibody response nor an effective mechanism for virus clearance but could infect other mice.^[30] I’ve known many parents with autistic children who told me they noticed the change in their child right after the MMR vaccine. Based on the nature of this vaccine being a triple live virus, I would have expected it to be notorious for triggering autism and the science tells us how this could be so,^[31] but it is not the only vaccine with potential to cause it.

You can even look into the term post-vaccinal encephalitis and complications of vaccination that present sometimes with neurologic and developmental defects following vaccinations of all kinds. As one paper states, “Similarly, although the encephalitis following vaccination against smallpox (post vaccinial encephalitis) is the typical example of encephalitis as a sequel to prophylactic inoculations, the term post-vaccinal should be used for the range of neurological disorders following vaccinations of all kinds.”^[32]

Therefore, it was already known that vaccination could induce neurological diseases of all kinds,^[33] and autism would be no different since it is immune-mediated.^[34] Autism is a broad spectrum, but at its very core it is driven by brain inflammation and immunodeficiency from para-infectious causes that adversely affect the brain in early development. They say neurologic complications from vaccination are rare, but that’s not necessarily true. What is rare are the vaccine injuries easily definable that can be placed into these boxes of diagnosis that fit their highly specific definition of what a vaccine-derived neurological complication “should” look like.

The reality is that the vast majority would fall within the immune tolerant spectrum in which inflammation is minimal and immune response is blunted. The characteristic nature of these injuries would fall within the range of low-level neuroinflammation described by Bechter and ignored by doctors and medical providers.^[35] Traub noted how the immune tolerant outcomes are nearly impossible to distinguish from the non-infected healthy subjects on a clinical basis because of how little inflammation is involved.^[36] Even their bloodwork comes back normal.^[37] These cases are actually the sickest cases but are ignored. Dr. Raymond Dattwyler, in a 1994 FDA meeting on Lyme disease and its potential vaccine, admitted the immunodeficient cases have a worse disease than those who have healthy immune systems:

Dr.O’BRIEN: “I was concerned about your last slide where you said there was a poor correlation between serologic response and clinical disease. And as I heard you to say, some people who mount better immune responses get worse disease. Did I hear you say that?”

DR. DATTWYLER: “No, no, I said the reverse. The better responses tended to have better response. […] the ones that failed to mount a vigorous response tended to do worse, clinically. So, there was an inverse correlation between the degree of serologic response and the outcome.”

“So, individuals with a poor immune response tend to have worse disease.”^[38]

To demonstrate that vaccine injuries can cause the same indistinguishable immune tolerance-like chronic disease, we can see in David H. Persing’s patent Method for Detecting B. burgdorferi Infection, where he clearly states vaccine failure looks indistinguishable from late stage Lyme disease:

Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure.^[39]

Since the adverse reactions to the Lyme disease vaccine (LYMErix) also fall in this category and look indistinguishable from late-stage Lyme disease,^[40] “vaccine failure” could also be defined to include vaccine injuries, in which case, the vaccine not only failed to protect, but failed to be safe. I believe this vague terminology “vaccine failure” was used on purpose to denote both.

Although autism spectrum disorders could potentially happen in rare instances from environmentally acquired viral infections depending of their HLA type, it is nearly guaranteed by overloading children who are already immunologically overburdened from the litany of vaccinations during infancy, especially a triple virus vaccine like MMR (Mumps, Measles, Rubella). Even more so if they had previously received the DTaP triple bacterial vaccine, HepB vaccine, and the very immunosuppressive COVID-19 vaccines.^[41]

The MMR vaccine contains three dry-frozen (lyophilized) viruses.^[42] Erich Traub’s German bioweapons lab had been studying this dry-freezing process for its potential for delayed reactivation of viruses following lyophilization.^[43] Imagine this from a biowarfare perspective, where you could attack a target population by freeze drying vaccine viruses that could serve as a ticking timebomb waiting to erupt, where such vaccines given to an enemy country would cause delayed reactivation of vaccine virus and destruction without them realizing it was the vaccine because it was significantly delayed from the time of vaccination.^[44] Traub’s Insel Riems team published minimal work on this in the open literature during the Second World War but by 1945 the Soviet Union had captured the lab and hauled off all of its WWII research,^[45] so we’ll never know what they discovered further about this dry-freezing process.

To further demonstrate why we should be concerned about the potential for vaccines (especially MMR) to cause autistic spectrum disorders via neurotropic viral infection, is because such reactivation of vaccine virus causing systemic infections were laid out by scientists and medical doctors from John Hopkins University and other universities in a 1999 paper Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue where they isolated vaccine strains of the virus from the brain of a dead infant killed by the vaccine. They admit that when a child has a poor immune response to the vaccine because of immunosuppression, the vaccine viruses reactivate, regain their virulence, and begin circulating and shedding for many months after the vaccination:

However, fatal infections have been documented in immunodeficient children vaccinated with these strains. The symptoms of infection occur many months after immunization, and the viruses isolated are similar to the original LA vaccine, suggesting that in the absence of an effective host immune response, persistent infection with the vaccine strain can lead to fatal disease. Viruses isolated from these children could potentially represent virulent revertants of the original LA vaccine.^[46]

This also shows, for the record, that many outbreaks of measles today could be traced to vaccinated persons who are unknowingly immunodeficient with persistent measles, mumps, and rubella vaccine virus infections but you can be sure they would keep that secret to prevent further vaccine hesitancy. Active infections from vaccine viruses have also been noted with rubella vaccine viruses reactivating in the immunodeficient, published in 2019 as Infectious vaccine-derived rubella viruses emerge, persist, and evolve in cutaneous granulomas of children with primary immunodeficiencies.^[47]

Healthcare providers do not test beforehand to see whether a child has these immune deficiencies before a vaccine is given because there are no tests to measure the immune tolerance spectrum as they do not consider this spectrum of disease a disease at all until the vaccine kills the person, then they just simply say the child was immunodeficient. Patients who try to get help for diseases that fall in the immune tolerant spectrum with low-level neuroinflammation are often referred to psychiatry as psychosomatic or imagining their disease (somatoform).^[48] Oftentimes these cases will show normal bloodwork, just as those infected by Lyme disease are immunosuppressed yet all their routine bloodwork comes back normal without evidence of active infection,^[49] but this has been admitted in research papers as seronegative disease.^[50] But the quote from the paper on measles vaccine viruses reactivating and causing fatalities proves that when immunodeficiency is present, the vaccine virus regains itself and starts new infections. These vaccine-derived persistent infections can circulate and shed from the vaccinated person to others and cause vaccine-derived outbreaks, as was noted in a 2022 publication Case report: Persistent shedding of a live vaccine-derived rubella virus in a young man with severe combined immunodeficiency and cutaneous granuloma.^[51]

The phenomenon of vaccine-derived outbreaks was also seen with polio vaccines causing vaccine-derived polio epidemics in a recent 2026 publication focused on how this affects vaccine safety, Polio outbreaks due to vaccine-derived viruses demand a re-definition of vaccine safety.^[52] Outbreaks of vaccine-derived measles, mumps, and rubella virus are guaranteed to occur because of how immunosuppressive the COVID-19 vaccines are. Many of those vaccinated are continuing to make spike protein months to years later.^[53] Further research on the COVID-19 vaccine shows it is seriously immunosuppressive and able to cause immune tolerance (immunodeficiency), as it was highlighted in a paper IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein. It says:

However, emerging evidence suggests that the reported increase in IgG4 levels detected after repeated vaccination with the mRNA vaccines may not be a protective mechanism; rather, it constitutes an immune tolerance mechanism to the spike protein that could promote unopposed SARS-CoV2 infection and replication by suppressing natural antiviral responses. Increased IgG4 synthesis due to repeated mRNA vaccination with high antigen concentrations may also cause autoimmune diseases, and promote cancer growth and autoimmune myocarditis in susceptible individuals.^[54]

The SARS-CoV-2 spike protein is what makes it so immunosuppressive, and it has been noted that SARS-CoV-2 virus infections are immunosuppressive, shown in a paper Severe immunosuppression and not a cytokine storm characterizes COVID-19 infections.^[55] To further show it is the spike protein itself, we can see the SARS-CoV-2 spike protein indeed stimulates the Toll-Like Receptors (TLR) of the immune system responsible for immunosuppression and immune tolerance, which happens through TLR2/1 and TLR2/6, demonstrated in SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway:

Notably, upon recognition of S[pike] protein, TLR2 dimerizes with TLR1 or TLR6 to activate the NF-κB pathway.^[56]

Stimulation of immune system toll-like receptors TLR2/1 and/or TLR2/6 are involved in immune tolerance, which includes T-cell exhaustion,^[57] and this is documented in several papers, with Toll-like receptor 2 controls expansion and function of regulatory T cells serving as particularly noteworthy.^[58] Once TLR2/1 and TLR2/6 are stimulated, a variety of mechanisms are responsible for the suppression that drives the immune system to tolerance or paralysis – such as upregulation of IL-10.^[59] Therefore, the COVID-19 vaccine-induced spike protein will have the exact same outcome for many of those vaccinated. Since the public health officials are recklessly giving children COVID-19 vaccines alongside other vaccines, oftentimes at the same time, the ability for profound immunodeficiency is not only very real but guaranteed.

If this is then followed by an MMR vaccination, we are ensuring a very dangerous situation not only for the child but also for others exposed to them by promoting vaccine-derived measles, mumps, and rubella outbreaks that are being wrongly blamed on vaccine hesitancy.^[60] What I am laying out here shows the exact opposite to be true.^[61] And this will also mean that the autism rate will skyrocket like never before – following the rollout of the COVID-19 vaccine in children – and we are indeed seeing just that.^[62]

Many public health officials and those with financial ties to vaccine manufacturers have repeatedly tried to debunk the idea that persistent measles virus was not present in MMR-vaccinated persons with autism. In one study, No Evidence of Persisting Measles Virus in Peripheral Blood Mononuclear Cells from Children with Autism Spectrum Disorder, they tested the blood for virus and concluded there was no persistent infection with the vaccine virus.^[63] But this would have been expected, because other news articles have admitted that “Measles is a stealth virus. It may look like it has cleared your body, but it can hide in your nervous system.”^[64] Therefore, this study looking at the blood is not sufficient. Other studies have tried to rule out the connection by looking at the gut and GI symptoms, claiming that autism must happen in a particular order with GI disturbances coming first, followed by autism:

If MMR is causally related to either GI disturbances or [autism] it should precede their onset. Similarly, if GI disturbances contribute to [autism] they should precede onset of [autism].^[65]

Here is the problem, autism does not necessarily have to happen in this particular order, and autism is not exclusively tied to gastrointestinal disturbance.^[66] Based on my knowledge of the immune tolerance spectrum, it would be expected that autism and GI disturbances would frequently happen in parallel but not exclusive to one another. They both fall in the general realm of immunodeficiencies within the immune tolerance spectrum in which a considerable variation of symptoms of immunodeficiency exist.^[67] GI disturbances are well known in people with immune deficiencies, it happens with many of the chronically ill who have tick-borne disease co-infections,^[68] and vaccine injuries.^[69] Therefore, it does not necessarily precede autism. It also means that in autism spectrum disorders, measles virus would not be consistently found in the GI tract. Reactivated herpesviruses also cause GI disturbances,^[70] and the herpesviruses could contribute to GI disturbances in some of the autistic cases in the total absence of MMR vaccination.^[71]

Autism is a brain disease but the immune system has been shown to be intricately involved in autistic spectrum disorders.^[72] Autoimmunity also falls in the immune tolerance spectrum, as it is found that primary immunodeficiencies and autoimmunity can happen simultaneously.^[73] That is because autoimmunity is not so much an overactive, supercharged immune system but an overwhelmed immune system that is also trying to attack pathogenic material that has fused itself to our tissues, organs, and brain.^[74]

Therefore, the GI disturbances that can accompany autism are merely co-factors of the overall immune deficiencies that accompany autism.^[75] These GI disturbances are not always present in autism and autism can also be present in the absence of MMR vaccination if the child is experiencing immunosuppression from prior vaccines like the COVID-19 vaccine, HepB vaccine, DTaP vaccine, Meningococcus B vaccine, or any other vaccine prior to the administration of or in the absence of an MMR vaccine.^[76]

It would also not be out of context for GI disturbances to start before administration of MMR vaccine in cases where autism was triggered by the vaccine, being that the vaccine served as the tipping point to trigger and activate the autistic spectrum disorders as the brain is attacked by the vaccine viruses and/or reactivated herpesviruses. So, because they were not able to verify Wakefield’s claim that autism is from measles vaccine virus given in the MMR vaccine followed by GI disturbances and then autism - in that particular order - that it simply could not be the cause of autism. This is a poorly constructed assumption, based on what we know of immune tolerance and immunodeficiencies and how the ensuing chronic disease unfolds in immune deficiencies.

Even though MMR vaccine could very well trigger autism in many of those vaccinated, it is not just MMR vaccines that have potential to trigger autistic spectrum disorders. All other vaccines, even the non-infectious antigen vaccines like the HepB vaccine, could potentially trigger autism by the vaccine antigen suppressing the immune system and reactivating dormant viruses.^[77] There are many papers on PubMed showing an association between autistic spectrum disorders and the common herpesviruses like HCMV,^[78] HHV-6,^[79] HSV,^[80] and the polyomaviruses that infected half the United States population in the 1950s and 60s from the continued use of contaminated polio vaccines.^[81] Therefore, in cases where no MMR was given, yet still developed autism, similar mechanisms could be at play with other vaccines and the subsequent immunosuppression and reactivation of dormant viruses and this is supported by available scientific literature.^[82]

However, there is one aspect of this that needs to be addressed because otherwise one would mistakenly conclude, like many other papers have, that there is no connection between these viruses and autistic spectrum disorders because both normal subjects and those with autistic spectrum disorder are equally infected by such viruses.^[83] This is a poor conclusion if one understood that standard PCR tests are not able to differentiate between latent infection and persistent slow virus infections.^[84] In many persistent infections the virus continues to maintain infection while maintaining viral loads far below those with active acute infections,^[85] while in other cases it remains a latent infection,^[86] the lines between one and the other are indistinguishable and this was noted with Human Papilloma Virus (HPV).^[87] This would explain why some researchers found no differences in viral content between those with neuropsychiatric disorders and healthy controls, as they were both infected by similar viruses, but each could be experiencing very different forms of the infection.^[88] One would be doing silent but significant harm, while the other is more or less inert and benign because of dormancy. Such concepts were discussed in an older 1957 conference Latency and Masking in Viral and Rickettsial Infections.^[89] This was then discussed in a follow-up conference the following year that Erich Traub attended in 1958 in Stockholm, Sweden for the Symposium on Latency and Masking of Viruses.^[90]

There are additional hurdles in assessing the true nature of these viruses in the body of autistic vs healthy subjects when depending on the presence of antibodies. That is because immune tolerant cases are infected but since the immune system is suppressed they lack a sufficient antibody response to the virus yet they are persistently infected.^[91]

Many latent viruses are neurotropic when reactivated, and so, like the MMR vaccine viruses, the human herpesviruses reactivating from immunosuppression can cause a very similar effect on the brain via neurotropic viral infections.^[92] Erich Traub had discovered how this could be utilized in biological weapons work disguised as vaccine research in his early Lymphocytic Choriomeningitis Virus (LCMV) experiments. In these experiments, he injected foreign antigens into the brains of mice to see if he could reactivate a dormant virus.^[93] He reactivated this virus and it spread to all the other mice.^[94] He realized that these reactivated viruses would be neurotropic and slowly destroy the brain and central nervous system and bring on neurological disease and slow chronic wasting diseases.^[95] They mirrored a similar process that could play out for the common human herpesviruses that most people have in latent form.

Additional factors that could greatly add and contribute to the autism picture are stealth infections like Borrelia burgdorferi (Lyme disease) and co-infections,^[96] Chlamydia pneumoniae, and especially mycoplasma.^[97] Mycoplasma becomes very relevant in the vaccine safety discussion because mycoplasma contamination of vaccines has been a major problem in the pharmaceutical industry, and its significance has been pointed out in the scientific literature to a limited extent.^[98] It is clear however that the general attitude within the vaccine industry in spending the required money to deal with it sufficiently is one of little enthusiasm or concern for public safety. Dr. Garth Nicolson, Ph.D., a prominent mycoplasma researcher, has discussed this in one of his lectures, citing a conversation he had with a vaccine manufacturer on a flight, and they started talking about mycoplasma. Eventually, he bluntly asks him why they don’t address this problem responsibly and the vaccine manufacturer’s response was telling. Nicolson said:

“We haven’t really, I think, reached any conclusion in the case of children with Autistic Spectrum Disorders but my guess is it will be related to the multiple vaccines that they received, either because of immunosuppression of these young patients who don’t have fully developed immune systems anyway, or to contaminants in the vaccines.

Now one of the papers that I use, often cite - is the fact that when commercial vaccines are checked for contaminants, one of the contaminants, that’s found quite often in commercial vaccines, is mycoplasma, [crowd participant: “In the vaccines?”] ...in the vaccines. Now you might say ‘well, why don’t they do something about this?’

Well, I just happened to, by chance, take a flight somewhere, I forgot where I was going, to fly back to Washington for one reason or another, and I happen to be with a, sitting next to, a vaccine manufacturer who was really mad because he got bumped out of first class. So he was riding back there with the rest of us and complaining, a blue streak and everything, and I started asking him where he was going and he was going to the FDA for someone.

So we actually started talking and I started telling him what we had found, and he started getting more and more nervous, as time went on until finally, I flat-out asked him I said “well I know that you know about this problem and I want to flat out ask you why don’t you test these vaccines for mycoplasma because I think this is a potential problem” and his immediate knee-jerk response was “what are you trying to do drive us out of business? I said ‘What do you mean try to drive you out of business I think it’s a matter of safety,’ then he started hedging and hawing, and making up excuses, and so on and so forth, and the fact of the matter is they don’t wanna test for these types of things because its EXPENSIVE to test for these types of infections, and quite frankly I think they’re afraid of what they might find.

...So, this was part of the whole problem of convincing authorities, convincing people that we need to look into these things, uh, much more seriously.”^[99]

The mechanisms of autistic spectrum disorders and many other neuropsychiatric/neurological disorders would seem a bit more apparent if we “followed the science,” like the work of those important players in the biological weapons game like Erich Traub, who made foundational contributions to the immunology of chronic disease, immune deficiencies, and the reactivation of neurotropic viral infections.^[100] If we “trust the science,” as they say, we can read between the lines and pull out all the contradictions and we can see that modern science and their figureheads like Anthony Fauci are not honest with us about many things. They failed to tell us that they were actively inducing immune tolerance on purpose with these vaccines – a very destructive process to the immune system – as a defense strategy.^[101] All evidence would suggest they were indeed trying to induce immune tolerance with the COVID-19 vaccine.^[102] They forgot to tell us the dangers of reactivating latent neurotropic viral infections even though they knew this could be involved in producing slow wasting diseases like Alzheimer’s Disease and other diseases where amyloids play a role.^[103]

I tend to think Andrew Wakefield’s conclusions were at least partially right in that MMR Vaccines can in fact cause autism but it does not seem to be specific to MMR vaccination. It could happen from other vaccines and the interaction between immune deficiency, reactivated viruses, and other co-infections. Its also not exclusively tied to GI disturbances.

More evidence suggests a coordinated attack on Wakefield was undertaken by people financially involved with the drug companies like GlaxoSmithKline (GSK), Merck and the British Medical Journal (BMJ) so they could squash the idea entirely.^[104] Andrew Wakefield may not be an angel but that doesn’t mean everything he was suggesting was fraudulent and unfounded. Whether one wants to believe or disbelieve he committed any level of fraud is neither here nor there in the actual question itself of whether vaccines can cause autism because none of my conclusions draw from his research.

All my conclusions were arrived at independently from other scientific literature without any need to draw from his original paper or findings. Erich Traub’s findings, serve as a critical and important starting point because all of Traub’s work on immune tolerance and virus reactivation play a very crucial role in understanding how many of the modern chronic diseases operate at a fundamental level from immune deficiencies complicated by the role that reactivated dormant viruses and co-infections like mycoplasma can play in enhancing the chronic disease.^{[105], [106]}

Somewhere along the way, the discussion of the vaccine’s role in autistic spectrum disorders was hijacked and run into the ground by ignoring these more insidious mechanisms and blaming it all on the metal adjuvants. I’m not arguing that the adjuvants are not toxic and can’t mirror symptoms of neurotropic viral infections, but we already have the basic underlying machinery mapped out in the literature for how autistic spectrum disorders generally work independant of metal adjuvants. Erich Traub demonstrated how it falls into this realm of immunodeficiencies by these immune tolerance/virus reactivation mechanisms without metal adjuvants of any kind. If anything, there is possibly further synergy between para-infectious mechanisms and metals, but autistic spectrum disorders would still happen even if all of the metal adjuvants were removed. The metal adjuvants were actually put in vaccines originally as a way to try and suppress the fungal, microbial and mycoplasmal contamination, so removing them would see a drastic rise in autism. The New York Times published an article in 2012 Vaccine Rule Is Said to Hurt Health Efforts, showing that adjuvants like thimerisol (and equally applicable to aluminum) were actually introduced into these vaccines to try and prevent fungal and bacterial contamination of commercial vaccines:

But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians […] They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay […] Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.^[107]

So, if those are considered the safest ingredients in the vaccine, what does that tell you about the main ingredients? First, in the early years of the vaccine safety debate, they tried to blame the thimerisol for autism, but that didn’t pan out as planned and then suddenly the debate shifted to aluminum. But it will keep happening regardless of whether aluminum or thimerisol is in the vaccines and the vaccine industry knows this. This is why they want the anti-vaccine movement to stay focused on specific metal adjuvants like thimerisol or aluminum that can always be replaced by other comparable adjuvants. If we were to attack the more insidious mechanisms of the antigens and the immunology behind the technology itself, the pharmaceutical industry would have to completely reconfigure vaccination and what immunity is and how it works. As of right now, they totally ignore the far-reaching implications of what immune tolerance means in relation to vaccine antigen, Infectious disease, and active immunity. If they acknowledged immune tolerance to viral and microbial antigen, they would find that vaccination is actually causing immune tolerance and profound immunodeficiencies rather than leaving us with true immunity.

The vaccine antigens are the culprits in triggering the tolerance-like immune deficiencies that precede autism and the vast number of adverse events also fall within the spectrum of immune tolerance with systemic reactivation of dormant viruses. It is why none of the vaccine injured are recognized but simply ignored because they fall within this diagnostic no man’s land. Modern physicians do not recognize non-specific symptoms lacking detectable inflammation and antibodies as recognizable manifestations of infectious disease. This is more so when it’s assumed to be from vaccines or stealth infections. Karl Bechter showed earlier in this article how the reactivated neurotropic viral infections are often left undiagnosed since they fall within this diagnostic blind spot.^[108] Yet leaving these problems unaddressed means the patient is then left to suffer a painful, devious infection without any recognition or treatment for a very real and seriously harmful disease.

But it gets worse, because the reactivation of dormant viruses and vaccine viruses that are neurotropic could potentially act as an infective wasting (prion) disease, as was shown in Traub’s studies of LCM Virus.^[109] Later, in 1964, Traub’s American friend John Hotchin published about the potential for these neurotropic viral infections to thoroughly destroy us like slow prion diseases:

The role of relatively ‘harmless’ viruses in the initiation of human late-onset [wasting] disease has long been suspected, but proof of this remains elusive. The occurrence of late disease in LCM [Virus]-[persistent tolerant infected] mice constitutes an example of an infective wasting disease, with an incubation period greater than half the normal expected life span of the host. This evidence strengthens the concept that other diseases of later life may, like some types of cancer, owe their origin, not to faulty genetics, but to a slowly acting but insidiously destructive virus.^[110]

Back in 1964, the reactivation of latent herpesviruses we’ve discussed was barely understood, and many of them had not been discovered yet. Epstein-Barr Virus (EBV) was discovered that year, and like the others, would be studied for its potential in many forms of cancer.^[111] Also, the eight human herpesviruses are often found as co-factors in diverse manifestations of chronic disease and neuropsychiatric disorders.^[112] Many papers exist showing routine vaccinations of all kinds can reactivate these viruses.^{[113], [114], [115]} Many papers also exist showing a potential link between the reactivation of these viruses, vaccine viruses, and the development of autistic spectrum disorders.^[116] Karl Bechter showed how this works and why it is ignored. Healthcare providers don’t pay any attention to these viruses in their effect on health due to it producing low-level neuroinflammation and lacking the diagnostic criteria responsible for the diagnosis of an infectious disease.^[117]

Besides, acknowledging these stealth infections would also expose major health risks with vaccination, so pharmaceutical companies and the top public health officials who have financial ties to each other have no desire to assess these risks. Our public health is compromised and influenced by corporate needs and foreign influence more than by our safety. This is why they so fiercely attack any claims of serious harms resulting from their multi-billion dollar industry that make tens of billions of USD per year globally.^[118]

Modern public health was setup to completely ignore all health problems that fall in the realm of immune tolerance – that is, chronic immune deficiency and chronic disease showing low-grade inflammation and poor antibody response. That’s why Western medicine gave the 1960 Nobel Prize for immune tolerance to Burnet and Medawar, making immune tolerance about organ transplant recipients while glossing over Traub’s findings relating to antigen and infectious disease.^{[119], [120]} They tell all of the vaccine injured and patients with stealth infections there is nothing wrong with them and that they’re imagining their symptoms.^[121]

I’ve met handfuls of people who became chronically ill after routine vaccinations of all kinds. The public health system simply ignores them unless they can classify it as autoimmune and other chronic disease manifestations that they can accurately measure as some syndrome or disorder. In turn, they make trillions of dollars in profits for treating these syndromes and disorders without acknowledged causes. It’s a win-win for the pharmaceutical giants to have these vaccines causing us further health problems because they can further profit off us without having to take any accountability.^[122] We allow them to by not realizing what is laid out in this article and not demanding change.

I was personally affected by a HepB vaccine in 8^th grade (1998), and following the vaccination I had ADHD/ADD, anxiety disorder, behavioral health problems, and other neuropsychiatric manifestations. I had no idea it was the vaccine until I was researching for The Sleeper Agent from 2017-2023 and found a congressional hearing from 1998 where other children had the same exact reaction.^[123] They simply ignore all of these potential harms, especially as it relates to the reactivation of neurotropic viruses that cause every neurological and psychiatric adverse effects imaginable.

I’m not against preventing disease if it is done safely and without harming the person, but I am wholeheartedly against it if it means we’re causing serious and often irreversible immunological harm to people while lying to them and telling them it is safe. I’m wholeheartedly against begging the public to get a harmful vaccine that could destroy their life, then throwing them to the wolves when they experience vaccine injuries and ignoring the devastating disease they have to carry from that point forward. That’s what our public health system did to us during COVID-19, and React-19.org was formed to address these vaccine injures as they were thrown to the wolves and ignored by public health.

Drug companies have created these harmful products that do serious harms while public health officials aid and abet them. The establishment and vaccine manufacturers deny and refuse to address the harms being done. Based on the scientific literature, there are serious problems not being addressed and those in public health are well aware of these mechanisms. Faulty studies have become the too commonplace response to all our grievances and concerns. So much so, that one might worry it is done on purpose to deflect any blame or accountability. If so, they’ve made establishment fraud into a fine art while having zero consideration or accountability for the adverse health effects it is having on billions of human lives.

They often say, “one death is a tragedy, a million deaths a statistic,” and the same could also be said of the robbed potential of so many who, rather than die, are forced to live out a painful, miserable existence. The pharmaceutical companies aren’t held liable for the failure of their products, so they don’t care either way, that’s why pharma successfully lobbied and handed that bill to the American taxpayers to handle through the National Vaccine Injury Compensation Program (VICP), created under the National Childhood Vaccine Injury Act of 1986.^[124]

The National Childhood Vaccine Injury Act of 1986 desperately needs to be repealed and drug companies need to be held accountable. Erich Traub’s discovery of immune tolerance in relation to antigen and infectious disease needs to become part of our modern immunology relating to infectious disease for public health or we are dooming our children to a very painful, demoralizing future that ensures they live the most miserable existence possible, and all the parents of the autistic children are getting older every day and will not be here forever. Who’s going to care for these severely autistic people and look out for them when the parents who were caring for them are gone? The corporations and governments have absolutely no consideration or care in the world for their safety or well-being… Am I the only one concerned? I certainly hope not…

^[1] Valsamakis, A et al. “Altered virulence of vaccine strains of measles virus after prolonged replication in human tissue.” Journal of virology vol. 73,10 (1999): 8791-7. doi:10.1128/JVI.73.10.8791-8797.1999

^[2] Shah, K, and N Nathanson. “Human exposure to SV40: review and comment.” American journal of epidemiology vol. 103,1 (1976): 1-12. doi:10.1093/oxfordjournals.aje.a112197

^[3] Al-Salihy, Adil Abdul-Rehman Siddiq. “Toward an immunological classification of autism spectrum disorder: A PRISMA-ScR-compliant scoping review.” Journal of neuroimmunology vol. 417 (2026): 578962. doi:10.1016/j.jneuroim.2026.578962

^[4] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

^[5] Croft, P B. “Para-infectious and post-vaccinal encephalomyelitis.” Postgraduate medical journal vol. 45,524 (1969): 392-400. doi:10.1136/pgmj.45.524.392

^[6] Wakefield, A J et al. “Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children.” Lancet (London, England) vol. 351,9103 (1998): 637-41. doi:10.1016/s0140-6736(97)11096-0

^[7] Nicolson, Garth L et al. “Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.” Journal of neuroscience research vol. 85,5 (2007): 1143-8. doi:10.1002/jnr.21203

^[8] report, Hub staff. “Russian Trolls, Twitter Bots Stoked Vaccine Debate by Spreading Misinformation, Study Finds.” The Hub, 24 Aug. 2018, hub.jhu.edu/2018/08/24/russian-trolls-bots-spread-vaccine-misinformation/.

^[9] Finnegan, A. W. (2023). The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. Trine Day.

^[10] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).

^[11] Annals of the New York Academy of Sciences: Volume 181, Issue 1. “Immunological Tolerance to Microbial Antigens.” The New York Academy of Sciences, May 1971, https://www.nyaspubs.onlinelibrary.wiley.com/toc/17496632/1971/188/1

^[12] Traub, E. Factors Influencing Specific Antibody Formation in Mice Persistently Infected with LCM virus. Zentralblatt Für Veterinärmedizin Reihe B, 28(2), 133-145 (1980,2010). doi:10.1111/j.1439-0450.1981.tb01748.x

^[13] Traub, E. Serological Evidence for Antigenic Variation in Brains of Mice Infected Persistently with the Virus of Lymphocytic Choriomeningitis. Zentralblatt Für Veterinärmedizin Reihe B, 27(9-10), 806-822. (1980, 2010). doi:10.1111/j.1439-0450.1980.tb02035.x

^[14] Traub, E. Observations on “Late onset disease” and Tumor Incidence in Different Strains of Laboratory Mice infected Congenitally with LCM Virus I. Experiments with Random-bred NMRI Mice. Zentralblatt Für Veterinärmedizin Reihe B, 22(9), 764-782. (1975, 2010). doi:10.1111/j.1439-0450.1975.tb00643.x

^[15] Traub, E. Observations on immunological tolerance and “Immunity” in mice infected congenitally with the virus of lymphocytic choriomeningitis (LCM). Archiv Fur Die Gesamte Virusforschung, 10(3), 303-314. doi:10.1007/bf01250677. (1960).

^[16] Traub, E. Serological Evidence for Antigenic Variation in Brains of Mice Infected Persistently with the Virus of Lymphocytic Choriomeningitis. Zentralblatt Für Veterinärmedizin Reihe B, 27(9-10), 806-822. (1980, 2010). doi:10.1111/j.1439-0450.1980.tb02035.x

^[17] Traub, E. Observations on immunological tolerance and “Immunity” in mice infected congenitally with the virus of lymphocytic choriomeningitis (LCM). Archiv Fur Die Gesamte Virusforschung, 10(3), 303-314. doi:10.1007/bf01250677. (1960).

^[18] Ibrahim, Hanan Mohamed et al. “HLA-B class I allele associations with neurological complications in pediatric SARS-CoV-2 infection: a retrospective observational study.” BMC pediatrics vol. 26,1 691. 25 Jul. 2026, doi:10.1186/s12887-026-07370-9

^[19] Byrne, D et al. “Yield of brain MRI in children with autism spectrum disorder.” European journal of pediatrics vol. 182,8 (2023): 3603-3609. doi:10.1007/s00431-023-05011-2

^[20] Bechter, Karl. “Virus infection as a cause of inflammation in psychiatric disorders.” Modern trends in pharmacopsychiatry vol. 28 (2013): 49-60. doi:10.1159/000343967

^[21] Belgamwar, R B et al. “Measles, mumps, rubella vaccine induced subacute sclerosing panencephalitis.” Journal of the Indian Medical Association vol. 95,11 (1997): 594.

^[22] Traub, E. & K. Beller. Untersuchungen uber die ansteckende Blutarmut der Pferde. II. Ubertragungsversuche. [Research on equine infectious anemia. II. Transmission experiments.] Archiv fur wiss. und prakt. Tier. 77:411-422. (1942) [Translated to English by A. Finnegan, 2019]

^[23] Landrigan PJ, Witte JJ. Neurologic Disorders Following Live Measles-Virus Vaccination. JAMA. 1973;223(13):1459–1462. doi:10.1001/jama.1973.03220130011003

^[24] Libero, Lauren E et al. “Persistence of megalencephaly in a subgroup of young boys with autism spectrum disorder.” Autism research : official journal of the International Society for Autism Research vol. 9,11 (2016): 1169-1182. doi:10.1002/aur.1643

^[25] Raz, Eytan. “Megalencephaly: Radiology Reference Article.” Radiopaedia, Radiopaedia.org, 23 July 2025, radiopaedia.org/articles/megalencephaly.

^[26] Lacour, M, and M Harms. “Gianotti-Crosti syndrome as a result of vaccination and Epstein-Barr virus infection.” European journal of pediatrics vol. 154,8 (1995): 688-9. doi:10.1007/BF02079084

^[27] Gentile, Ivan et al. “Prevalence of Congenital Cytomegalovirus Infection Assessed Through Viral Genome Detection in Dried Blood Spots in Children with Autism Spectrum Disorders.” In vivo (Athens, Greece) vol. 31,3 (2017): 467-473. doi:10.21873/invivo.11085

^[28] Traub, E. Epidemiology of Lymphocytic Choriomeningitis In A Mouse Stock Observed for Four Years. Journal of Experimental Medicine, 69(6), 801-817. doi:10.1084/jem.69.6.801. (1939).

^[29] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).

^[30] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

^[31] Valsamakis, A et al. “Altered virulence of vaccine strains of measles virus after prolonged replication in human tissue.” Journal of virology vol. 73,10 (1999): 8791-7. doi:10.1128/JVI.73.10.8791-8797.1999

^[32] Croft, P B. “Para-infectious and post-vaccinal encephalomyelitis.” Postgraduate medical journal vol. 45,524 (1969): 392-400. doi:10.1136/pgmj.45.524.392

^[33] Douglas J Lanska MD MS MSPH. Neurologic complications of vaccination. In: Lewis SL, Editor-in-Chief. MedLink Neurology. San Diego: MedLink, LLC. Available at www.medlink.com. Updated: December 2, 2025.

^[34] Al-Salihy, Adil Abdul-Rehman Siddiq. “Toward an immunological classification of autism spectrum disorder: A PRISMA-ScR-compliant scoping review.” Journal of neuroimmunology vol. 417 (2026): 578962. doi:10.1016/j.jneuroim.2026.578962

^[35] Bechter, Karl. “Virus infection as a cause of inflammation in psychiatric disorders.” Modern trends in pharmacopsychiatry vol. 28 (2013): 49-60. doi:10.1159/000343967

^[36] Traub, E. Ueber den Einfluß der latenten Choriomeningitis-Infektion auf die Entstehung der Lymphomatose bei weißen Mause [On the Influence of Latent Choriomeningitis Infection on the Development of Lymphomatosis in White Mice]. Zentrl. Bakt. I. Orig. 147 (16). 1-25. (1941). [Translated to English by A. Finnegan, 2019]

^[37] Traub, E. Observations on immunological tolerance and “Immunity” in mice infected congenitally with the virus of lymphocytic choriomeningitis (LCM). Archiv Fur Die Gesamte Virusforschung, 10(3), 303-314. doi:10.1007/bf01250677. (1960).

^[38] Food and Drug Administration. Vaccines and Related Biological Products Advisory Committee: Lyme Disease Vaccine Trial Design. Department of Health and Human Services, 22 June 1994. Transcript. Copy of text viewable here: https://web.archive.org/web/20140716100646/http://www.actionlyme.org/1994_FDA_MEETING_LYMERIX.htm

^[39] Persing, David H. Method or PCR Detection of Borrelia burgdorferi Infection. United States Patent US6045804A, April 04, 2000.

^[40] VRBPAC (Vaccines and Related Biological Products Advisory Committee) of the Food and Drug Administration. 2001. Minutes, January 31. Retrieved from: https://web.archive.org/web/20190816101909/http://www.actionlyme.org/2001_FDA_LYMErix_Transcripts.pdf

^[41] Erich Traub had noted how the immune tolerant phenomenon correlates to the very similar descriptions of immune paralysis following large doses of pneumococcal polysaccharide, and it was also induced through multiple overlapping co-infections infecting at the same time, which Traub’s mentor Karl Beller had shown him in putting his paper together on the rickettsioses of animals. Traub then noted how the same immune tolerance-like phenomenon could be found in infectious catarrh (“mixed infections”), indicating that antigen overload is often the driving factor in triggering the immune tolerance phenomenon.

^[42] “M-M-R II Vaccine: Package Insert .” Drugs.Com, www.drugs.com/pro/m-m-r-ii-vaccine.html. Accessed 13 Aug. 2026.

^[43] RUSKA, H: Zur Frage der Potenzierung von Bakteriophagenlösungen durch Zerschäumen [On the question of the potentiation of bacteriophage solutions by foaming]. Kolloid-Zeitschrift 110 (1948), S. 175-177 [paper submitted in 1945, not published until 1948.]

^[44] Eberle, Henrik. “Ein Wertvolles Instrument”: Die Universität Greifswald Im Nationalsozialismus. Bohlau Verlag, 2015.

^[45] Central Intelligence Agency (CIA) Intelligence Reports: THE BACTERIOLOGICAL RESEARCH INSTITUTE ON THE ISLAND OF RIEMS. CIA-RDP83-00415R002200020014-9. Central Intelligence Agency (CIA), Reading Room, 2011. Retrieved from: https://www.cia.gov/library/readingroom/docs/CIA-RDP83-00415R002200020014-9

^[46] Valsamakis, A et al. “Altered virulence of vaccine strains of measles virus after prolonged replication in human tissue.” Journal of virology vol. 73,10 (1999): 8791-7. doi:10.1128/JVI.73.10.8791-8797.1999

^[47] Perelygina, Ludmila et al. “Infectious vaccine-derived rubella viruses emerge, persist, and evolve in cutaneous granulomas of children with primary immunodeficiencies.” PLoS pathogens vol. 15,10 e1008080. 28 Oct. 2019, doi:10.1371/journal.ppat.1008080

^[48] Tavel, Morton E. “Somatic Symptom Disorders without Known Physical Causes: One Disease with Many Names?” The American journal of medicine. U.S. National Library of Medicine, October 2015. https://www.ncbi.nlm.nih.gov/pubmed/26031885

^[49] TruthCures. “LYME CRYME.” YouTube. YouTube, September 2, 2016.

^[50] Gustafsson, Freja et al. “Borrelia afzelii-associated seronegative Lyme neuroborreliosis in an immunocompromised patient.” Diagnostic microbiology and infectious disease vol. 113,3 (2025): 116999. doi:10.1016/j.diagmicrobio.2025.116999

^[51] Bonner, Kimberly E et al. “Case report: Persistent shedding of a live vaccine-derived rubella virus in a young man with severe combined immunodeficiency and cutaneous granuloma.” Frontiers in immunology vol. 13 1075351. 8 Dec. 2022, doi:10.3389/fimmu.2022.1075351

^[52] John, T Jacob et al. “Polio outbreaks due to vaccine-derived viruses demand a re-definition of vaccine safety.” The Lancet. Microbe vol. 7,3 (2026): 101290. doi:10.1016/j.lanmic.2025.101290

^[53] Boros, László G et al. “Long-lasting, biochemically modified mRNA, and its frameshifted recombinant spike proteins in human tissues and circulation after COVID-19 vaccination.” Pharmacology research & perspectives vol. 12,3 (2024): e1218. doi:10.1002/prp2.1218

^[54] Uversky, Vladimir N et al. “IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein.” Vaccines vol. 11,5 991. 17 May. 2023, doi:10.3390/vaccines11050991

^[55] Remy, Kenneth E et al. “Severe immunosuppression and not a cytokine storm characterizes COVID-19 infections.” JCI insight vol. 5,17 e140329. 3 Sep. 2020, doi:10.1172/jci.insight.140329

^[56] Khan, Shahanshah et al. “SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway.” eLife vol. 10 e68563. 6 Dec. 2021, doi:10.7554/eLife.68563

^[57] Schietinger, Andrea, and Philip D Greenberg. “Tolerance and exhaustion: defining mechanisms of T cell dysfunction.” Trends in immunology vol. 35,2 (2014): 51-60. doi:10.1016/j.it.2013.10.001

^[58] Sutmuller, Roger P M et al. “Toll-like receptor 2 controls expansion and function of regulatory T cells.” The Journal of clinical investigation vol. 116,2 (2006): 485-94. doi:10.1172/JCI25439

^[59] Mabrey, F Linzee et al. “TLRs in COVID-19: How they drive immunopathology and the rationale for modulation.” Innate immunity vol. 27,7-8 (2021): 503-513. doi:10.1177/17534259211051364

^[60] Adeoye, Adekunle F et al. “The 2025 United States Measles Crisis: When Vaccine Hesitancy Meets Reality.” Cureus vol. 17,7 e88196. 17 Jul. 2025, doi:10.7759/cureus.88196

^[61] Valsamakis, A et al. “Altered virulence of vaccine strains of measles virus after prolonged replication in human tissue.” Journal of virology vol. 73,10 (1999): 8791-7. doi:10.1128/JVI.73.10.8791-8797.1999

^[62] St Victor, Rosemarie et al. “Rise in Autism Spectrum Disorder Diagnoses: A Comparative Analysis of Pre-pandemic and Pandemic Periods.” Cureus vol. 16,9 e70167. 25 Sep. 2024, doi:10.7759/cureus.70167

^[63] D’Souza, Yasmin et al. “No evidence of persisting measles virus in peripheral blood mononuclear cells from children with autism spectrum disorder.” Pediatrics vol. 118,4 (2006): 1664-75. doi:10.1542/peds.2006-1262

^[64] Szabo, Liz. “Measles Infections Pose Far More Risks than Most Realize, Including a Fatal Neurological Complication.” NBCNews.Com, NBCUniversal News Group, 20 Feb. 2024, www.nbcnews.com/health/kids-health/measles-infection-symptoms-longterm-risks-rcna138583.

^[65] D’Souza, Yasmin et al. “No evidence of persisting measles virus in peripheral blood mononuclear cells from children with autism spectrum disorder.” Pediatrics vol. 118,4 (2006): 1664-75. doi:10.1542/peds.2006-1262

^[66] Wasilewska, Jolanta, and Mark Klukowski. “Gastrointestinal symptoms and autism spectrum disorder: links and risks - a possible new overlap syndrome.” Pediatric health, medicine and therapeutics vol. 6 153-166. 28 Sep. 2015, doi:10.2147/PHMT.S85717

^[67] Rose, Destanie R et al. “T cell populations in children with autism spectrum disorder and co-morbid gastrointestinal symptoms.” Brain, behavior, & immunity - health vol. 2 100042. 26 Jan. 2020, doi:10.1016/j.bbih.2020.100042

^[68] Crystal , Jennifer. “Gastrointestinal Issues with Lyme Disease.” Global Lyme Alliance, 21 June 2021, www.globallymealliance.org/blog/gastrointestinal-issues-with-lyme-disease.

^[69] Ajmera, Kunal et al. “Gastrointestinal Complications of COVID-19 Vaccines.” Cureus vol. 14,4 e24070. 12 Apr. 2022, doi:10.7759/cureus.24070

^[70] Goodgame, R W. “Viral infections of the gastrointestinal tract.” Current gastroenterology reports vol. 1,4 (1999): 292-300. doi:10.1007/s11894-999-0112-5

^[71] Chen, Li-Chi et al. “Risk of Neurodevelopmental Disorders Following the Herpesviral Infection in Preschooler Children.” Autism research : official journal of the International Society for Autism Research, e70336. 28 Jul. 2026, doi:10.1002/aur.70336

^[72] Gagliano, Antonella et al. “The Immune/Inflammatory Underpinnings of Neurodevelopmental Disorders and Pediatric Acute-Onset Neuropsychiatric Syndrome: A Scoping Review.” International journal of molecular sciences vol. 26,16 7767. 11 Aug. 2025, doi:10.3390/ijms26167767

^[73] Schmidt, Reinhold E, et al. “Autoimmunity and Primary Immunodeficiency: Two Sides of the Same Coin?” Nature Reviews. Rheumatology, U.S. National Library of Medicine, 19 Dec. 2017, https://www.ncbi.nlm.nih.gov/pubmed/29255211

^[74] Serraino, Carolyn. “Infections and Pathogens as Triggers of Autoimmune Disease.” Global Autoimmune Institute “ Empowering Solutions for Autoimmune Disease, 30 Apr. 2025, www.autoimmuneinstitute.org/research_updates/infections-and-pathogens-as-triggers-of-autoimmune-disease/.

^[75] Griffith, Dorsey. “Immune System and Gastrointestinal Deregulation Linked with Autism | Microbiome Research Working Group.” UC Davis Microbiome Research Working Group, 17 Apr. 2018, microbiome.ucdavis.edu/news/immune-system-and-gastrointestinal-deregulation-linked-autism.

^[76] Akkelle, Bilge S et al. “Gastrointestinal Manifestations in Children with Primary Immunodeficiencies: Single Center: 12 Years Experience.” Digestive diseases (Basel, Switzerland) vol. 37,1 (2019): 45-52. doi:10.1159/000492569

^[77] Chen, Li-Chi et al. “Risk of Neurodevelopmental Disorders Following the Herpesviral Infection in Preschooler Children.” Autism research : official journal of the International Society for Autism Research, e70336. 28 Jul. 2026, doi:10.1002/aur.70336

^[78] Pesch, Megan H et al. “Autism Spectrum Disorder Diagnoses and Congenital Cytomegalovirus.” Pediatrics vol. 153,6 (2024): e2023064081. doi:10.1542/peds.2023-064081

^[79] Nicolson, Garth L et al. “Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.” Journal of neuroscience research vol. 85,5 (2007): 1143-8. doi:10.1002/jnr.21203

^[80] Ganguli, Sourav, and Pavithra L Chavali. “Intrauterine Viral Infections: Impact of Inflammation on Fetal Neurodevelopment.” Frontiers in neuroscience vol. 15 771557. 10 Nov. 2021, doi:10.3389/fnins.2021.771557

^[81] Lintas, Carla et al. “Association of autism with polyomavirus infection in postmortem brains.” Journal of neurovirology vol. 16,2 (2010): 141-9. doi:10.3109/13550281003685839

^[82] Binstock, T. “Intra-monocyte pathogens delineate autism subgroups.” Medical hypotheses vol. 56,4 (2001): 523-31. doi:10.1054/mehy.2000.1247

^[83] Min, Shishi et al. “No Increased Detection of Nucleic Acids of CNS-related Viruses in the Brains of Patients with Schizophrenia, Bipolar Disorder, and Autism Spectrum Disorder.” Schizophrenia bulletin vol. 49,3 (2023): 551-558. doi:10.1093/schbul/sbad003

^[84] Watzinger, F et al. “Detection and monitoring of virus infections by real-time PCR.” Molecular aspects of medicine vol. 27,2-3 (2006): 254-98. doi:10.1016/j.mam.2005.12.001

^[85] Luzyanina, T et al. “Low level viral persistence after infection with LCMV: a quantitative insight through numerical bifurcation analysis.” Mathematical biosciences vol. 173,1 (2001): 1-23. doi:10.1016/s0025-5564(01)00072-4

^[86] Traub, E. Ueber den Einfluß der latenten Choriomeningitis-Infektion auf die Entstehung der Lymphomatose bei weißen Mause [On the Influence of Latent Choriomeningitis Infection on the Development of Lymphomatosis in White Mice]. Zentrl. Bakt. I. Orig. 147 (16). 1-25. (1941). [Translated to English by A. Finnegan, 2019]

^[87] Ryser, Marc D et al. “IPVS Consensus Statement on The Natural History of Cervical Human Papillomavirus Infection.” The Journal of infectious diseases vol. 233,4 (2026): 735-744. doi:10.1093/infdis/jiaf574

^[88] Min, Shishi et al. “No Increased Detection of Nucleic Acids of CNS-related Viruses in the Brains of Patients with Schizophrenia, Bipolar Disorder, and Autism Spectrum Disorder.” Schizophrenia bulletin vol. 49,3 (2023): 551-558. doi:10.1093/schbul/sbad003

^[89] Walker, Duard L., et al. Latency and Masking in Viral and Rickettsial Infections: Proceedings of a Conference Held at the University of Wisconsin Medical School, 1957. Burgess, 1958.

^[90] Traub, E.: Panel discussion, Symposium on Latency and Masking of viruses VII. Internat. Congr. für Microbiol. Stockholm 1958

^[91] Traub, E. Observations on immunological tolerance and “Immunity” in mice infected congenitally with the virus of lymphocytic choriomeningitis (LCM). Archiv Fur Die Gesamte Virusforschung, 10(3), 303-314. doi:10.1007/bf01250677. (1960).

^[92] Bechter, Karl. “Virus infection as a cause of inflammation in psychiatric disorders.” Modern trends in pharmacopsychiatry vol. 28 (2013): 49-60. doi:10.1159/000343967

^[93] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).

^[94] Traub, E. An Epidemic in A Mouse Colony Due to The Virus of Acute Lymphocytic Choriomeningitis. Journal of Experimental Medicine, 63(4), 533-546. doi:10.1084/jem.63.4.533. (1936).

^[95] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

^[96] Bransfield, Robert C. “Neuropsychiatric Lyme Borreliosis: An Overview with a Focus on a Specialty Psychiatrist’s Clinical Practice.” Healthcare (Basel, Switzerland) vol. 6,3 104. 25 Aug. 2018, doi:10.3390/healthcare6030104

^[97] Nicolson, Garth L et al. “Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.” Journal of neuroscience research vol. 85,5 (2007): 1143-8. doi:10.1002/jnr.21203

^[98] Armstrong, Shayn E et al. “The scope of mycoplasma contamination within the biopharmaceutical industry.” Biologicals : journal of the International Association of Biological Standardization vol. 38,2 (2010): 211-3. doi:10.1016/j.biologicals.2010.03.002

^[99] Nicolson, Garth L “Weaponized Mycoplasmas - Dr Garth Nicolson” Why we don’t vaccinate (Rumble Channel). 2023 https://rumble.com/v34jssy-weaponized-mycoplasmas-dr-garth-nicolson (discussion regarding Mycoplasma in vaccines starts around 54:00)

^[100] Finnegan, A. W. (2023). The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. Trine Day.

^[101] Medzhitov, Ruslan et al. “Disease tolerance as a defense strategy.” Science (New York, N.Y.) vol. 335,6071 (2012): 936-41. doi:10.1126/science.1214935

^[102] Uversky, Vladimir N et al. “IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein.” Vaccines vol. 11,5 991. 17 May. 2023, doi:10.3390/vaccines11050991

^[103] HOTCHIN, J, and D N COLLINS. “GLOMERULONEPHRITIS AND LATE ONSET DISEASE OF MICE FOLLOWING NEONATAL VIRUS INFECTION.” Nature vol. 203 (1964): 1357-9. doi:10.1038/2031357a0

^[104] “Corrections: Wakefield’s Article Linking MMR Vaccine and Autism Was Fraudulent | the BMJ.” BMJ, 2011, www.bmj.com/content/342/bmj.d1678

^[105] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

^[106] Nelson, J B. “INFECTIOUS CATARRH OF MICE : I. A NATURAL OUTBREAK OF THE DISEASE.” The Journal of experimental medicine vol. 65,6 (1937): 833-41. doi:10.1084/jem.65.6.833

^[107] Tavernise, Sabrina. “Experts Say Thimerosal Ban Would Imperil Global Health Efforts - The New York Times.” The New York Times , 17 Dec. 2012, www.nytimes.com/2012/12/17/health/experts-say-thimerosal-ban-would-imperil-global-health-efforts.html.

^[108] Bechter, Karl. “Virus infection as a cause of inflammation in psychiatric disorders.” Modern trends in pharmacopsychiatry vol. 28 (2013): 49-60. doi:10.1159/000343967

^[109] Traub, E. Observations on “Late onset disease” and Tumor Incidence in Different Strains of Laboratory Mice infected Congenitally with LCM Virus I. Experiments with Random-bred NMRI Mice. Zentralblatt Für Veterinärmedizin Reihe B, 22(9), 764-782. (1975, 2010). doi:10.1111/j.1439-0450.1975.tb00643.x

^[110] HOTCHIN, J, and D N COLLINS. “GLOMERULONEPHRITIS AND LATE ONSET DISEASE OF MICE FOLLOWING NEONATAL VIRUS INFECTION.” Nature vol. 203 (1964): 1357-9. doi:10.1038/2031357a0

^[111] EPSTEIN, M A et al. “VIRUS PARTICLES IN CULTURED LYMPHOBLASTS FROM BURKITT’S LYMPHOMA.” Lancet (London, England) vol. 1,7335 (1964): 702-3. doi:10.1016/s0140-6736(64)91524-7

^[112] Carneiro, Vanessa Cristine de Souza et al. “Family Herpesviridae and neuroinfections: current status and research in progress.” Memorias do Instituto Oswaldo Cruz vol. 117 e220200. 21 Nov. 2022, doi:10.1590/0074-02760220200

^[113] Walter, R et al. “Reaktivierung von Herpesviren-Infektionen durch Impfungen: Evidenz oder Koinzidenz?” [Reactivation of herpes virus infections by vaccination: evidence or coincidence?]. Schweizerische medizinische Wochenschrift vol. 130,44 (2000): 1685-8.

^[114] Shafiee, Arman et al. “Herpesviruses reactivation following COVID-19 vaccination: a systematic review and meta-analysis.” European journal of medical research vol. 28,1 278. 10 Aug. 2023, doi:10.1186/s40001-023-01238-9

^[115] Richardson-May, James et al. “Reactivation of herpes simplex keratitis following vaccination for COVID-19.” BMJ case reports vol. 14,9 e245792. 7 Sep. 2021, doi:10.1136/bcr-2021-245792

^[116] Binstock, T. “Intra-monocyte pathogens delineate autism subgroups.” Medical hypotheses vol. 56,4 (2001): 523-31. doi:10.1054/mehy.2000.1247

^[117] Bechter, Karl. “Virus infection as a cause of inflammation in psychiatric disorders.” Modern trends in pharmacopsychiatry vol. 28 (2013): 49-60. doi:10.1159/000343967

^[118]“Vaccines Market Size, Share: Global Growth Report [2034].” Fortune Business Insights, www.fortunebusinessinsights.com/industry-reports/vaccines-market-101769. Accessed 14 Aug. 2026.

^[119] Silverstein, Arthur M. “The curious case of the 1960 Nobel Prize to Burnet and Medawar.” Immunology vol. 147,3 (2016): 269-74. doi:10.1111/imm.12558

^[120] Dinter, Z. Persönaliches, Begegnungen mit Erich Traub.[Personal Encounters with Erich Traub] Berl. Munch. Tier. Woch. 96. 70-72. (1984)

^[121] Kellner, R. “Psychosomatic Syndromes, Somatization and Somatoform Disorders.” Psychotherapy and psychosomatics. U.S. National Library of Medicine, 1994. https://www.ncbi.nlm.nih.gov/pubmed/8121976

^[122] Nicolson, Garth L “Weaponized Mycoplasmas - Dr Garth Nicolson” Why we don’t vaccinate (Rumble Channel). 2023 https://rumble.com/v34jssy-weaponized-mycoplasmas-dr-garth-nicolson

^[123] Hepatitis B Vaccine: Helping or Hurting Public Health? | Congress.Gov | Library of Congress, Retrieve from: www.congress.gov/event/106th-congress/house-event/LC66602/text. Accessed 14 Aug. 2026.

^[124] “About the National Vaccine Injury Compensation Program.” HRSA, www.hrsa.gov/vaccine-compensation/about. Accessed 14 Aug. 2026.

See the interview here:

https://drtenpenny.com/ttf-afinnegan/

It was great speaking with Dr. Tenpenny about The Sleeper Agent and all about Traub and other mechanisms of what he discovered, being “immune tolerance” and “virus reactivation” and so much more. It was also nice to be able to inform people about who was running Vaccine Safety and Review at the FDA, no other than M. P. Chumakov’s son Konstantin Chumakov. This is a huge red flag if you know about who his father is…

^{**For the full length of this article be sure to view in Substack instead of email. Video can be viewed below}

This article is a deep dive into the origins of Lyme disease as a manmade event. This is going to be an extensive article and a response to my favorite critic who works hard trying to “debunk” the connection to Erich Traub and biowarfare. I am going to address further the relationship between the Lyme Borreliosis clade of Borrelia that cause Lyme disease and its relationship to the bird borreliosis - Borrelia anserina. I am going to explain some of the factors surrounding the taxonomy and the sudden, deep split between Borrelia anserina and the Lyme clade. I’m going to address the fact that taking a microorganism that has been used to one primary host and vector (birds and soft-bodied Argas ticks) for millions or more years and then suddenly giving it entirely new characteristics it did not have before, introducing it into a new vector with broad-spectrum host infectivity and challenging it with successfully overcoming the immune defenses of hundreds of new animal hosts released on multiple continents would put an enormous amount of selection pressure on the spirochete and it would be forced to either rapidly evolve or be phased out of existence.

A well-known critic on X known as Henjin, who formerly went by the icon of a Mongolian wearing the flag of Finland, who many are already acquainted with, prides himself thinking he has single-handedly demolished my book The Sleeper Agent, but did a terrible job debunking it. For those who don’t know, Henjin is an anonymous X account that appeared in 2023 from Finland, according to Open VAET’s exchange with the digital Mongolian in Dunning-Kruger Illustrated, ASMR Explained & Bad Non-Official Czech Data we learn the following about his background in an exchange about the COVID vaccine:

In the following developments and controversies, Henjin (ex Mongol_fi), 8-bits data mixer masquerading as “experienced conspiracy theorist”, produced yet another of these Chat-GPT analytic flows that he masters like no one else, in his urge to demonstrate that the jabs are working as intended.

The character appeared on the Twitter-scene end 2023, and his only endorsed conspiracy to date is “all Jews are bad”. Don’t ask him to justify this view, or that makes you a “baby truther” only worthy of his despise. [1]

Despite posing as a “truther,” he viciously defends the COVID vaccine and a natural origin for SARS-CoV-2 and other suspicious biological agents with the ferocity of a ruthless Mongolian warrior. He is the Genghis Khan of the digital space. His method of fighting back is using Ai to reinforce the establishment talking points, but since this usually doesn’t go so well, smear tactics tend to be his primary approach, like a baby smearing feces on as much of everyone’s name and work as he possibly can. This sounds quite like the same approach the biodefense industry uses to keep people quiet, not questioning potential acts of bioterrorism or thinking critically.[2] Reinforce establishment science using bad information to push the official position and attack you and try to make you look crazy for suggesting it.[3]

Normally, I would not pay any attention to such trolls but I find some of Henjin’s criticisms relating to my book productive and helpful in clarifying further, rewording or reshaping my reconstruction, and if I have something wrong, I believe in correcting it. However, as far as this point is concerned with the Lyme clade and Borrelia anserina, which is his main criticism of my work, I find the truth about my reconstruction on the origins of Lyme disease from Borrelia anserina greatly strengthened instead of disproven. To be fair, I can understand why at first glance it seems like what I’m saying is such a stretch to him, but when we unravel all the many dynamic factors involved in my reconstruction, it shows far more complexity that most if not all small-scale laboratory experiments would completely fail to capture or replicate and it would be easy to lose sight of so many factors involved that are easily not taken into account in the larger picture.

Being as sick as I am, it’s often hard to keep up with rapidly putting out content like other content creators to please all the subscribers and especially those who pay, but Henjin’s criticism brings me motivation to keep putting out more material to counter his antics (or Ai’s), so thank you Henjin and his team of Ai LLMs for at least bringing me the continuous drive to write more.

Anyway, Henjin claims to have debunked The Sleeper Agent by pointing out the so-called ~25% divergence between Borrelia burgdorferi B31 and the bird borreliosis Borrelia anserina, in a section of his website Did Borrelia anserina become Borrelia burgdorferi? Response by Grok.[4] It is, in his mind, the Achilles’ heel that disproves The Sleeper Agent, but more than anything else, I would argue that it only further strengthens my reconstruction of events that it was engineered from the bird borreliosis (Borrelia anserina). Thank you Henjin for pointing this out to me, as it explains like no other some of the highly unusual factors and anomalies surrounding the Lyme clade and Borrelia anserina as a very recent event in highly unusual manmade conditions.

There was a growing demand to remodel this spirochete specifically in 1930s Germany to serve as a more suitable animal model for the study of syphilis, and in order to accomplish this, the spirochete would have to be entirely remodeled, and the man who had the most promising expertise, talent, and originality to make that happen was Erich Traub.

While diving deeper into this, I’ve noticed some additional contradictions in the “slow, natural evolution” argument for the Lyme clade that would point towards it not developing slowly or naturally. How it went from being totally absent in the 19^th and early 20^th century to suddenly becoming the most abundant form of Borrelia found throughout the globe is a telling anomaly. My reconstruction argues that the Lyme clade was totally absent all the way until the Second World War, and its rise and spread was a very recent event with mankind offering its helping hand in times of war.[5] So let’s begin…

Borrelia anserina and the Lyme Clade: A Morphological Match

For those unaware, there are generally only two main clades (groups) of Borrelia, the Relapsing Fever clade,[6] and the Lyme Borreliosis clade, sometimes termed Borrelia burgdorferi sensu lato (this includes several species known to cause Lyme disease, such as Borrelia afzelii, Borrelia garinii, Borrelia japonica, among others), and recently a third group has been proposed called the Reptile-Echidna Group (REP),[7] barely sitting beyond the Relapsing Fever Group with some additional Lyme-like traits, but this group could very well have been a later and recent emergence long after the Lyme group had established itself. In my book The Sleeper Agent, I put forward the Lyme clade as an emergence from a completely remodeled Borrelia anserina,[8] which is a bird borreliosis that sits in the Relapsing Fever group of Borrelia but doesn’t quite cluster so tightly together as the other Relapsing Fever Borrelia.[9]

I want to point out some notable elements that exist between Borrelia anserina, the Relapsing Fever clade of Borrelia, and the Lyme clade of Borrelia. Of all the Relapsing Fever (RF) group, Borrelia anserina sits closer to the Lyme Borreliosis group than all other Relapsing Fever Borrelia at the 16S rRNA gene and shares a nearly identical morphology with Borrelia burgdorferi,[10] and since the rest of the Lyme clade is so similar to Borrelia burgdorferi the same applies to these other Borrelia in the Lyme clade.[11] Despite these close parallels between the Lyme clade and Borrelia anserina, Borrelia anserina is classed with the Relapsing Fever (RF) group based on it being genetically closer to the Relapsing Fever Borrelia and causing a similar acute disease, even though morphologically Borrelia anserina is quite distinct from the other Relapsing Fever Borrelia and sort of forms its own little group within the Relapsing Fever clade.[12]

Not only does Borrelia anserina share a very close relationship to the Lyme clade when we’re talking morphology since they are nearly identical, but Borrelia anserina even shares unique flagellar epitopes with Borrelia burgdorferi not found in the mammalian Relapsing Fever Borrelia,[13] along with a host in birds,[14] even though the Lyme clade seems to produce an immune tolerant-like carrier state instead of causing fatal acute disease in birds like Borrelia anserina does.[15]

Henjin claims that a ~25% divergence between Borrelia anserina and Borrelia burgdorferi make it impossible that Borrelia burgdorferi and the Lyme clade could have come from Borrelia anserina in the span of a few years but I will show you in this article why not only does my position stand, but why a stark divergence is exactly what would be expected in such a drastic challenge to its survival under the intense manmade selection pressure. All of this being done on multiple continents in a very short time frame at a critical time in the biological arms race, exposing the re-engineered spirochete to a variety of different ecosystems across the globe simultaneously.

Henjin’s entire argument to speak against this as a manmade event uses simple math to calculate how long it would take for Borrelia to change by simple point mutations based on currently estimated mutation rates in a niche it has already adapted itself to while totally leaving out a dynamic of other factors that can dramatically change a microorganism under the right conditions. When giving a microorganism entirely new hosts, vectors, resistance genes, tropisms, and even changing the disease it causes, even if much of the heavy lifting is done through plasmids, this can set the stage for massive unprecedented genomic evolution once released into various ecosystems far and wide. This could change the pathogen dramatically even into new species within a very short time.

The fact that Borrelia anserina and the Lyme clade are nearly indistinguishable in morphology while the other Relapsing Fever Borrelia are so different is an interesting fact. For those unaware, morphology is the scientific study of form, structure, and the internal components of living organisms; in other words - its physical characteristics. It examines how each of the individual elements are configured to create a functional, identifiable picture of the whole microorganism. For spirochetes, being that they look like tiny corkscrew spiral-shaped worms, the morphology takes note of the length, wavelength, number of flagella, pointed or blunted ends, thickness, and sheath layers. This is characterized and catalogued for each individual species of Borrelia spirochetes, with papers often phrased as morphological characterization.

Morphology in animals was the way evolutionary placement was done in the days before genetics, and since then genetics have been added as complementary factors to the higher life forms, and now plays a big part in microbiology.[16] Borrelia anserina is morphologically quite different from all the other Relapsing Fever Borrelia in that the other Relapsing Fever spirochetes are notably thicker and contain far more flagella that are not sheathed and have sharply pointed ends.[17] From Hovind-Hougan’s paper A Morphological Characterization of Borrelia anserina (green/red colored outlines and text was added by me):

Up to now, very few types of Borrelia anserina have been catalogued and studied extensively. This could be very significant in terms of the genetic distances because since Borrelia burgdorferi sensu lato can vary up to ~2% in difference at the 16S rRNA gene between species,[18] with known strains of Borrelia anserina varying within its own species up to ~1.3%. But even still, this ~3.6-4% divergence cited between Borrelia burgdorferi sensu lato and Borrelia anserina is not much of a big leap since those within the Lyme clade can vary up to about half that. The bioengineering Traub was skilled in during his career would have been able to achieve that especially in forced environments with a multi-pathogen cocktail and alternating animal and tick passages, imparting antibiotic resistance, among other factors whereby it completely changes hosts, vectors, disease, tissue tropisms, and so on.

Henjin’s own graph shows that a ~2% variation within Borrelia burgdorferi sensu lato exists, but then contradicts himself by saying that if Borrelia burgdorferi was a weaponized Borrelia anserina, it should be 99.99% similar to the progenitor strain Borrelia anserina, but his own colorful graph shows even current strains of Borrelia anserina vary up to about ~1.3% at the most conserved gene. He also assumes by default that the Borrelia anserina strains from 1939 are the same and have not changed at all since that time. Here is his vibrant and colorful graph:

Before, I had considered that Traub may have weaponized several different types of Lyme disease spirochetes, but it’s also possible it was just merely one strain that diverged into many new species as a direct result of the global distribution and various ecosystems they established in and diversified further within those ecosystems based on a variety of different factors and dynamics from the life they live there.

Being an entirely remodeled Borrelia anserina to have merely every facet of its former life changed dramatically (new hosts, vector, tissue tropisms, and disease-causing characteristics), it would undergo a period in the beginning once released across the globe whereby it functions under emergency rules not typical of today’s well-adapted Borrelia burgdorferi, such as activating its newly imparted RpoS (master stress and host adaptation regulator) and SOS response system in order to adapt itself and transform its genome in a very short time, which you will read about later in this article. All of the criteria used to separate bacterial species would be affected by the sophisticated bioengineering I propose occurred, since nearly every element of Borrelia anserina was targeted for change.

Strains of Borrelia anserina have not been extensively studied or sequenced, and we have no sequence information going back to the 1939 strains Erich Traub and his protégé were in possession of.[19] Kari Hovind-Hougan stated in the 1995 paper that at that time all the different strains and types of Borrelia anserina have not been extensively studied or catalogued:

[…] Further comparative studies on the morphology, metabolism, and antigenic and genetic characters of different B. anserina strains are needed before the necessary criteria for a full description of the type species of the genus Borrelia can be given.[20]

Despite this need for further study, work on Borrelia anserina nearly dropped off the map after the 90s and no other paper on its morphological characterization exists. Only 13 papers were published on Borrelia anserina on PubMed after the 90s, and much of their information draws on much older literature. While some papers have claimed that Borrelia anserina can be distinguished from Borrelia burgdorferi by being longer generally,[21] there are also some strains of Borrelia burgdorferi that are just as long so it’s not really an absolute marker of difference.

The Lyme Clade: Most Abundant Borrelia on the Planet

One interesting anomaly within the Borrelia evolution discussion is that although Borrelia burgdorferi and the Lyme clade of Borrelia is the most abundant Borrelia on the planet,[22] being orders of magnitude more abundant than all of the Relapsing Fever Borrelia, and despite early researchers vigorously searching the globe to find and catalogue all the different forms of Borrelia up to the discovery of Borrelia burgdorferi and the Lyme clade, there was never a single sample found that matched the same morphology as the Lyme clade other than Borrelia anserina, otherwise, they would have either noted this new species and its similarity to Borrelia anserina (then known as Spirochaeta gallinarum), or they would have thought Borrelia anserina had a much larger host range than birds because it would have been mistaken for Borrelia anserina due to the nearly indistinguishable match morphologically.

The other Relapsing Fever Borrelia spirochetes are considerably different than Borrelia anserina and the Lyme clade. They are noticeably thicker, have sharply pointed ends, and have far more flagella than the Lyme clade and Borrelia anserina.[23] So, one would think if the Lyme clade had been slowly evolving over millions of years and is orders of magnitude more abundant than all other forms of Borrelia, someone would have at least found one sample of it before the Cold War era in the many hundreds of animals it infects.

Some evidence suggests that it may have been isolated in the early 1950s in patients with multiple sclerosis,[24] but was made controversial in academic circles,[25] especially after a second discovery of it in 1957.[26] It was claimed that the results could not be replicated but since my reconstruction shows that at this time they were actively trying to cover up the spread of these agents filtering through the population after Traub’s activity in Project Paperclip, it makes some interesting coincidences. It might explain the overlap to how similar controversies exist today within medical and science circles on the many aspects of Lyme disease, since it was being kept secret. After all, John Loftus claimed in his book The Belarus Secret, based on what his biodefense source had said:

[…] The Lyme disease outbreak in America was monitored secretly under the cover of a New England health study. [27]

Niche Factors and Host Switching in Species Diversification

There is one species within the Lyme clade that sits noticeably closer to Borrelia anserina in overall percentage of conserved proteins, Borrelia chilensis, which is only 12.8% divergent.[28] Its niche is an area around Chile with just two known hosts and one vector in Ixodes stilesi.[29] But this really doesn’t tell us much now that Borrelia burgdorferi sensu lato is distributed globally. Especially so if the spirochete changes considerably depending on the ecosystem, and might be part of the reason why the Lyme clade evolved into so many new genospecies from a single ancestor, which I have put forward as coming from a remodeled Borrelia anserina released onto multiple continents and ecosystems within the span of several years.

This mirrors what scientists are now beginning to see; each specific geographic location and continent adds to the Lyme clade diversification, though it is not to say that certain species can’t remain constant across multiple continents, such as Borrelia burgdorferi sensu stricto which has a large network spanning multiple continents rather than being isolated to a small particular niche and continent.

One paper, Borrelia bavariensis: Vector Switch, Niche Invasion, and Geographical Spread of a Tick-Borne Bacterial Parasite, studying the ecological factors and niche surrounding the Lyme clade species Borrelia bavariaensis considered that even one host switch from birds to mammals could have caused the divergence from Borrelia garinii into the new species Borrelia bavariensis, and this is coming from a scientist in the field:

Throughout its very extensive geographic range in Eurasia B. bavariensis is associated only with small mammals, implying that a host switch occurred at some time in the past that allowed, or perhaps even was the cause of the divergence of B. bavariensis from B. garinii. [29a]

Henjin at one point tried to debunk the Borrelia anserina connection by comparing it to a simple laboratory adaptation study from a human-adapted strain of Staphlyococcus aureus to infect sheep (ruminants) and presents the mutation rates after 400 passages where there were only about 8 mutation rates per sample and uses that to speak against my reconstruction. [29b]

This is a terrible comparison, since first off, this is a highly controlled and smooth laboratory adaptation that completely removes the vast dynamic of factors involved in my reconstruction, and secondly, Staphylococcus aureus already has a long history with ruminants, and what makes this a particularly bad example is that there is already another paper showing radical genomic remodeling in Staphylococcus aureus subspecies anaerobius due to a host switch from the very same host to the very same animal (human to ruminants) that occurred at some point in the distant past, where they believe a new subspecies formed because of it:

S. aureus subsp. anaerobius formed a distinct clade on a long branch within the S. aureus subsp. aureus diversity but was not genetically allied to any particular clonal complex that has been previously assigned. These data indicate that S. aureus subsp. anaerobius emerged from an unknown S. aureus lineage likely after a human to ruminant host-switch event that occurred over a millennium ago. [29c]

Henjin’s simple laboratory adaptation experiments are terrible comparisons to the dynamic situation I am presenting. When the entire argument that “Borrelia burgdorferi could not have come from Borrelia anserina” is based solely on the genome distance alone and an assumed slow-clock model of evolution under an assumed fixed mutation rate of small-scale point mutations as though they stay constant and gradually form new species slowly, it has serious limitations and almost sounds absurd because it totally fails to consider just how dynamic and unpredictable the life of a microbe is under different forms of stress, selection pressure, host and vector switching, and transitions of all kinds. There are instances in bacteria like that seen in the Lyme clade of Borrelia where it can function under completely different rules under selection pressure, rather than by fixed and steady small-scale mutations, they have backup strategies in certain circumstances that allow them to quickly evolve based on a dynamic set of factors.

Furthermore, a host switch, for example, is not a gradual process but a very quick and rapid process, not to mention, the limitations inherent in sequencing Borrelia spirochetes are very real and aren’t currently sufficient for resolving complex bacterial genomes like that seen with the Lyme Borreliosis clade, so its not exactly a settled area of science where looking at genome data alone tells you definitive histories and relationships other than being a general guide, which is exactly how we should treat it.

The consensus view tries to say Lyme disease has always been here using misleading science, yet they tend to try to blame climate change for the sudden expansion of it as a recent event.[30] However, it makes a lot more sense when explained through the lense of my reconstruction of events where totally remodeling Borrelia anserina gave it the necessary conditions to rapidly evolve in ways unthinkable to modern science. It would be an entirely unique set of factors that have never been studied in small-scale limited laboratory adaptations to study the vast evolutionary dynamics acquired in introducing a bioengineered spirochete into diverse ecosystems across the globe simultaneously. It is especially interesting that we see strains of the Lyme clade coming out of Japan, since Germany was sharing chemical and biological warfare advances with their Axis allies in Japan during World War II.[31]

Uncoordinated Phylogeography for Borrelia burgdorferi and Ixodes scapularis

One interesting aspect of the recent emergence of Lyme disease in the black-legged tick (Ixodes scapularis) that contradicts the slow evolution and emergence of Lyme disease as a natural event was highlighted in a paper noting that the evolutionary relationship between Borrelia burgdorferi and its tick vector Ixodes scapularis is contradictory, shown in a 2010 paper Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis:

Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.[32]

All the way up to the 1950s the black-legged tick was not a known transmitter of any known human diseases,[33] even though according to the slow evolution theory of it evolving over millions of years the Lyme disease spirochete should have been by this time at least found, and more so, found to be increasing, since it is now the most abundant Borrelia spirochete found throughout the globe and yet not a single sample was declared until 1982.[34]

The going argument is that deforestation is responsible for its sudden rise due to the Ixodes scapularis tick but like the above paper shows, Borrelia burgdorferi’s population structure, evolutionary history, and historical biogeography are all contrary to its arthropod vector. They have attempted to explain the anomaly of uncoordinated phylogeography by saying it’s because of birds carrying it long distances, such as has been put forward in “Diverse Borrelia burgdorferi strains in a bird-tick cryptic cycle,”[35] but that would mean birds had been spreading it far and wide despite the deforestation and it should have at least been discovered somewhere far before its 1982 discovery.

In light of this, and what follows in this paper, there are inconsistencies with the slow, natural evolution theory and its sudden explosion to become the most dominant form of Borrelia on the planet and I put forward why a man-made event explains its appearance and anomalies better than any other argument. One paper “Studies on Exotic Ixodes Ticks (Ixodoidea, Ixodidae) from United States Navy and Army Activities” shows there was a clear interest by the military in this genus of tick and therefore were a likely candidate for simulant testing studies.[36]

Limitations and Hurdles in Whole Genome Sequencing for Borrelia

Before we go any further, we must address that the ~25% divergence cited between Borrelia anserina and Borrelia burgdorferi may not be entirely accurate since there are still hurdles standing in the way of Whole Genome Sequencing (WGS) for Borrelia. Even with so-called pure culture growth medium to grow the spirochetes, which contain bovine and rabbit serum, along with antibiotics and yeast, along with human sources of contamination, all of which can introduce genetic information from foreign sources and potential contamination of the medium which is a well-known problem in laboratory work.[37]

This is even more so for the calculation of mutation rates estimated from field samples done through shotgun sequencing, mixing samples with an overwhelming presence of “exogenous DNA (which may also include commensal bacteria, endosymbionts, and environmental microbes) renders shotgun sequencing inefficient and cost-prohibitive,” making the limitations in whole genome sequencing from field samples especially problematic when it comes to Borrelia spirochetes.[38] I don’t think Henjin relied on any of the samples done with shotgun sequencing in his main comparisons of the genomes but may have drawn from them in his discussion of mutation rates for Borrelia in the wild.

Both sequencing from field samples and pure cultures can introduce artificial distance in the final genome along with assembly artifacts (sequences stitched together erroneously in machine-driven algorithmic reconstruction), culture bias (strains cultured in labs degrade and are a streamlined version of its wild type), among other setbacks.[39] It also relies on short-read sequences which are not sufficient and has been stated that “Short-read sequencing makes it impossible to fully resolve complex microbial genomes.”[40] Borrelia burgdorferi could probably qualify as one of the most complex microbial genomes of all, and Henjin’s entire argument is based on this fragile data alone.

I may discuss the limitations in whole genome sequencing for Borrelia more deeply in another article, because it is a significant fact to point out when someone relies on genome data alone as though it is absolutely concrete and pristine when there are significant hurdles in the way of precision for Borrelia spirochetes. However, I don’t want to overstate the importance of this here because the genetic distance is not a hurdle to my reconstruction but entirely expected. But it would be right to bring attention to these very real limitations which can create artificial distance not present in the wild spirochetes if we want to be realistic about precision and exact about numbers and percentages involved.

For this article, anyway, I’ll give Henjin the benefit of the doubt and treat the ~25% divergence as fully accurate. The deep split between Borrelia burgdorferi and Borrelia anserina represents a big jump. Average laboratory work is unlikely to produce this strictly under laboratory conditions mirroring much of the common bioengineering of today. However, Traub’s bioengineering was quite different than what is used today, and in the lab is not where I claim the big divergence actually happened, and I did not say that it was due to the animal passages per se, especially not for animals it was already adapted to. My reconstruction has it that it was a variety of original and very sophisticated bioengineering techniques including the use of a complex mix of infectious agents (multiple bacteria, blood parasites, viruses, bacteriophages, mollicutes, etc.) probably done through alternating animal passages in a variety of different animals and its new vector, gave it the tools to rapidly evolve, and it did so once it was released into the various ecosystems across the globe simultaneously. Especially so when formerly Borrelia anserina was used to just one host and vector (birds and Argas soft-bodied ticks) for a very, very long time.

Genetic distance does not automatically translate to having to happen slowly over millions of years. When there is no need for a bacteria to change much in a given system, it won’t, but in certain conditions it could change dramatically and very quickly. Certain bioengineering techniques can give a microorganism the necessary tools it needs to allow for much more accelerated rapid evolution once released into diverse ecosystems with hundreds of new hosts across the globe.[41] This would result in an ecological shock that could bring rapid evolution to the spirochete in quick jumps,[42] especially with the very unusual and extraordinary circumstances I present in this paper.

Henjin tries to debunk this using math on simple point mutations and calculating how many years it would take according to a set mutation rate which totally fails to understand how these microorganisms operate in the wild and in dynamic situations. Borrelia does not simply rely on small point mutations for its evolution in all instances. These are small mutations it undergoes as small scale maintenance to a niche and ecosystem it’s already adapted to, so the changes it needs to make are small. Remodeling Borrelia anserina on the other hand, to produce a different kind of disease it never produced before, changing tissue tropisms, vectors, and hundreds of new hosts brings a crisis and ecological shock to the spirochete in which it has to respond by a completely different set of rules and this has been shown in the literature, some of which is available in the citation section of this article.

In one paper “Diversity of 16S rRNA genes within individual prokaryotic genomes” researchers found an unusual discovery in which strains of Borrelia afzelii from the Lyme Borreliosis clade had two copies of its 16S rRNA gene that showed only about an 80% similarity to each other. [42a] One copy was considered functional, while the more divergent copy was interpreted as a pseudogene. This finding is interesting because 16S rRNA genes are normally highly conserved within species. While the exact evolutionary reason for this duplication and divergence remains unclear, it shows that there may be a lot about the genetics of Borrelia burgdorferi sensu lato that we don’t yet understand and presents evidence to suggest that perhaps the Borrelia genus is capable of far more plasticity and divergence than we give it credit for.

BLAST Database Limitations and Blindspots

Henjin also claims that if Borrelia burgdorferi had acquired foreign DNA from other sources he should be able to do a BLAST (Basic Local Alignment Search Tool) and find any matching segment from other genomes uploaded to the GenBank database, but he completely fails to understand the limits of BLAST, and plus we have the fact that Borrelia burgdorferi’s survival strategy under intense selection pressure makes use of entirely different rules than it normally utilizes like segmental gene conversion and an SOS response network affecting the entire genome where it is able to chop up, reshuffle, recombine, and repackage chains of genetic sequences from both its own internal genes and foreign DNA when the need arises.[43][44] When you add to this the complexity of a multi-pathogen cocktail surrounded by mycoplasma gene shuttles and bacteriophages, the capacity for genomic rearrangement and diversity becomes immense, many of which BLAST can miss.

Borrelia burgdorferi and the Lyme clade certainly could have segments, however small, containing genetic information imparted by other viruses and microorganisms, but the sequences are so short and fragmented it can easily be missed, not to mention, Borrelia burgdorferi has cross-reactivity to many other infectious diseases,[45] and antibody cross-reactivity with many viral infections,[46] and if genetic material inherited by any foreign viruses or bacteria are at all plausibly involved in creating this cross-reactivity they can be chopped up and recombined to such an extent that they are missed by doing a BLAST.

Borrelia burgdorferi also has antigens that can mimic host tissue, as pointed out in “Molecular mimicry and Lyme borreliosis: a shared antigenic determinant between Borrelia burgdorferi and human tissue,” so there is also this aspect relating to the hundreds of new mammalian hosts adding additional complexity if new variants were able to recombine plasmids to mimic certain host tissue on a molecular level. [47] I’m not claiming host DNA was incorporated into the spirochete, but I’m showing that the host certainly might affect the spirochete in unique ways such as repackaging plasmids to favor such mimicry traits, and if so, the main chromosome would have made regulatory adjustments to properly control these new plasmid-encoded traits.

If it were true that you could locate every piece of genetic information imparted by Borrelia burgdorferi via gene transfer from other bacteria and viruses, scientists would have been all over this and matched everything they could find from foreign sources in BLAST. It would have become a major part of the study of bacterial phylogeny. It would be an immense undertaking and there would be many hurdles standing in the way of accurately mapping out any foreign DNA inherited over the last 100 years. There are instances where they have found genetic material on the linear chromosome, part of its main genome, they believe to be from viruses, and this occurred in the telomeres where they found material they think may have come from the poxvirus family.

This was demonstrated in “Linear plasmids of Borrelia burgdorferi have a telomeric structure and sequence similar to those of a eukaryotic virus,” where they hypothesize that at some point through horizontal gene transfer it may have inherited material from the poxvirus family.[48] The sequence similarity was at 67% for African Swine Fever and a comparable percentage for Vaccinia Virus, but you’re not necessarily going to have a cleanly matching sequence because of how it can inherit small fragments of the segment, plus viruses can change dramatically over time, and also due to the fact that Borrelia is able to chop up and recombine the segment to suit its own particular needs, therefore, much of the genetic information it inherits from other sources is going to be labeled a mismatch or background noise and not picked up in BLAST:

Although this seems to imply it is involved in the plasmids only, this is actually part of the Borrelia chromosome, but it makes up the complex segmented genome that is so characteristic of Borrelia. Back when that paper was written, the genome hadn’t been fully sequenced and they were still trying to figure out what to make of some of the linear plasmids that functioned like minichromosomes and they stated:

These observations, and the finding that the Borrelia chromosome migrates in pulsedfield electrophoresis gels as a linear molecule of 950 kb, raise the possibility that the linear plasmids are actually minichromosomes. [48]

Yet, later on you can see this was part of the main chromosome that makes up its segmented genome, published in “Telomeres of the linear chromosomes of Lyme disease spirochaetes: nucleotide sequence and possible exchange with linear plasmid telomeres.” [48a] Although it is not specific to the Lyme clade, my point in bringing it up is to demonstrate that foreign material can enter the main chromosome and become part of the genome, and still be entirely missed in BLAST searches. However, I would argue that it’s quite possible to have been viral material given to the Lyme clade which then spread to the rest of the genus in the last century, because it is only on a certain part of the right end of the chromosome which is much more fluid and swaps genetic material with the plasmids regularly and since gene transfer is common between species of Borrelia, it could easily have been transferred to the rest of the genus through genetic transfer relatively quickly, since the entire point of gene transfer is to acquire favorable fitness traits, and as Casjens et al. stated there was historical exchange happening between plasmid and chromosome:

These observations suggest that there has been historical exchange of genetic information between the linear plasmids and the right end of the linear chromosome. [48b]

Where was Henjin on that possible viral inheritance discovery? He must have missed it since he’s relying on BLAST alone, and therein lies the limitation of BLAST searches, they are often too fragmented to be matched, or perhaps he thought was only relevant to plasmids since he has no understanding of the complex bacterial genome of Borrelia, but here we had Barbour and Hinnebusch claiming viral material was probably inherited by Borrelia into its genome through genetic transfer at some time. Their hypothesis does not appear to be the result of a BLAST search but from their knowledge of these viruses cited in several papers and when they manually compared the two, as they state that no match was found through GenBank, “No similarities were found between the Borrelia telomeric sequences and other viral or prokaryotic sequences in the GenBank data base.”

Certainly, any foreign DNA inherited through transfer could be in highly fragmented form or chopped up and recombined so as to be unrecognizable in its final form when re-assembled by Borrelia burgdorferi sensu lato. As for its genome, it would have underwent significant upgrades following the sophisticated bioengineering that Traub was overseeing at Insel Riems once released and spread across the globe. In fact, it was mandatory for this to occur in order to become the sophisticated microorganism the Lyme spirochetes became because Borrelia anserina was not built to regulate the dynamic and complex system that the Lyme clade would later showcase.

Many of the viruses Traub was working with at Insel Riems have not been uploaded or sequenced, the older strains can be very different than what is available today when the same kind of virus is sequenced. Since viruses are constantly changing, it makes sequencing very difficult to match to certain isolates back in time. These are not static viruses, they are highly volatile and constantly changing in the wild environments. With LCM Virus, for example, it was noted by Traub that the virus mutates so rapidly that it makes replicating experiments difficult, due to the fact that the virus can change so much up to the time of future experiments.[49] This once again points out how limited BLAST data can be.

Tick-Borne Superinfection and Immune Deficiency

My reconstruction of events told in The Sleeper Agent shows Erich Traub had learned how to incorporate a myriad of infections all rolled into one tick and would co-infect together like a Russian-doll cocktail of infectious disease, a complex polymicrobial superinfection.[50] Erich Traub was known for mixing pathogens together in other instances in his adaptation work. He learned under his mentor Karl Beller in 1939 how a mix of Babesia, Ehrlichia, Bartonella, Rickettsia, and Leishmania could create a complex infection in a dog, while also noting it was possible in some instances for Borrelia spirochetes to be transmitted by hard-bodied ticks.[51] It’s strange that later on in America we see the very same cocktail of infections in the ticks with slight modification substituting Leishmania with a completely remodeled Borrelia spirochete.[52]

With a Russian-doll cocktail of infectious agents all growing together, major genetic exchange is happening, and since these agents are able to induce immune tolerance in many of their hosts, it raises the mutation rate significantly because rapid mutations happen in the immunosuppressed. During the COVID-19 pandemic, it was found that one immunosuppressed person infected with SARS-CoV-2 had 20 mutations in a single infection.[53] While viruses have a higher mutation rate than bacteria,[54] both still mutate much faster in the immunosuppressed.[55] In an immunosuppressed syphilis patient co-infected with HIV spreading the disease around, it was found that two different types of the syphilis spirochete (Treponema pallidum) combined after genetic recombination and underwent intrahost evolution bringing confirmation that bacteria don’t always change slowly. It shows for the record that quick jumps in evolution can happen under the right conditions when he said in the video:

We have documentation going back decades that this particular bacteria changes slowly. But we’ve now been able to directly observe that different strains can and will recombine genetically to create new strains. It’s not to say that this has never happened before, it’s just that we now have evidence of seeing it first-hand.[56]

While I mention the possibility of Traub utilizing viruses and co-infecting pathogens of all kinds, it’s also very possible he incorporated multiple species of Borrelia together in the bioengineering process to re-engineer Borrelia anserina. This would make use of a similar concept and one that Erich Traub was entirely familiar with utilizing like mixing multiple pathogens in the same medium to facilitate accelerated adaptation. He famously did this with Foot-and-Mouth Disease Virus when adapting it to chicken eggs, where he mixed 10 strains in one egg. The mixing of multiple types of Borrelia would have brought forth favorable opportunities for adaptation through recombination, plasmid exchange, and rapid selection of variants better suited to new hosts, vectors, and tissues.

No published scientific research available has ever replicated and accurately studied the unusual factors I am proposing surrounding the Lyme Borreliosis clade of Borrelia as a manmade event. We cannot compare the ecological dynamics to linear simple and controlled laboratory studies or limited animal adaptations because they in no way reflect the vast dynamic of factors in the wild on multiple continents with unique ecosystems growing in complex polymicrobial superinfections in immune tolerant hosts. Using an average estimated mutation rate for established bacteria from field samples totally misses the point.

With the unusual factors laid out in my reconstruction occurring at scale across the globe in diverse ecosystems, this is where I suggest the ecological shock and evolutionary crisis occurs to demand rapid unprecedented evolution of the spirochete. Traub did not adapt the spirochete to these animals one by one; he more likely identified a way to give broad-spectrum host infectivity by various methods all rolled together, but a select number of diverse animal adaptations could have certainly been involved (such as cattle, horse, mice, rodents, etc.). Traub probably learned some of the common factors through his study of agents like Borna Disease Virus,[57] Influenza,[58] and LCM Virus,[59] which are able to infect many, many different animals as broad-spectrum pathogens and zoonotic agents. Furthermore, these factors were not merely dependent on plasmids alone for doing this. Numerous papers show a layered chromosomally driven master control system which is fully at work in the dynamic of mammalian infection for Borrelia burgdorferi. [60] [61]

Erich Traub’s Expertise on Virus-Bacteria Interactions

When it came to adaptation and bioengineering, Erich Traub was known for using unusual and very original methods and it’s why he was particularly sought after for his knowledge of preparations for biological warfare and his intelligence file is very specific about this.[62] He also had a particular interest in virus-bacteria interactions, and this is not an abstract position.

During World War II, Insel Riems was already knee-deep in the study of bacteriophages and their morphologies and uses,[63][64] also with Mycoplasma which can act as gene shuttles,[65][66][67] and when grown together in high-density pathogen cocktails in selective animal passaging, Traub and his Insel Riems team had the expertise, the means, and the capacity to facilitate sophisticated bioengineering techniques for making an entirely new class of biological warfare agents. Borrelia can most certainly assimilate and use genetic material from foreign sources including other bacteria, viruses, and beyond, but today’s Lyme clade is so well-adapted it probably has much less need to at the current time.[68] As the Insel Reims work during World War II was highly secretive work, much of it would be kept secret just as classified research is today and was probably decades ahead of the open academic science of those times.

But they were going even deeper than this. During his time at Insel Riems during World War II, Traub and his team, including Werner Schäfer and Gerhard Schramm documented that Newcastle Disease Virus can sometimes assume highly pleomorphic forms under certain conditions, including elongated particles with a tail-like structure resembling that of a bacteriophage.[69] Although that paper wasn’t published until 1949, it specifically states in the paper it was research done when the three were together at Insel Riems during the Second World War. This was within just a few years from his 1940 paper on Bovine Papular Stomatitis Virus where he had filtered the virus through broth containing Serratia marcescens bacteria and noted that some of the bacteria had retained pathogenic material from the virus and caused disease in livestock when he infected the livestock with bacteria held back after filtering the virus.[70]

Strangely, many years later in the Soviet Union’s biowarfare program, which is the country that inherited all of Insel Riems’s World War II research, The Soviet Union talked about creating double pathogens with promotor viruses integrated within the plasmids of bacteria, discussed in The Soviet Biological Weapons Program: A History by the late Harvard Professor Raymand A. Zalinskas and Milton Leitenberg, they cited Soviet bioweaponeers discussing the creation of plague bacterium that harbored virulent Venezuelan Equine Encephalomyelitis (VEE) from within its plasmids that would be released when an antibiotic like tetracycline was taken and destroyed the bacteria.[71] Further evidence shows that this idea was not merely theoretical, but actively being pursued and accomplished by American researchers in 1964 at Caltech when they published Polyoma Virus: Production in Bacillus subtilis,[72] and by German researchers from the Max-Planck Institute in Tübingen when Pamela Abel and T. A. Trautner published The Formation of an Animal Virus Within a Bacterium:

The availability in this laboratory of a subviral entity, essentially the viral nucleic acid, of vaccinia virus (ABEL, 1963), as well as a system whereby competent B. subtilis cells could be infected with the DNA of a B. subtilis phage and subsequently produce whole phage particles (FÖLDES and TRAUTNER,1963), prompted us to expose the bacteria to the subviral entity and see whether complete vaccinia virus particles could be produced. This paper reports the successful outcome of these experiments.[73]

Was Erich Traub already creating new lysogenic-like systems within bacteria using pathogenic viruses in a similar way to prophages or proviruses? Or using them in non-conventional ways to be bacteriophage-like? In 1961, in a paper on Eastern Equine Encephalomyelitis Virus (EEE), Traub noted the ability for viruses (prophages are bacterial viruses) to integrate into the genomes of bacteria and replicate with the bacteria, seeming to play the role of bacterial genes, even though he was making parallels to explain the immune tolerance phenomenon in bacterial immunity, deep knowledge of these mechanisms and their applications were clearly within his expertise conceiving original methods and preparations for biological warfare:

The prophage in lysogenic bacteria (virus nucleic acid, genetic substance of the virus) is closely associated with the bacterial genome. It is non-infectious and does not multiply or reproduce itself independently. Instead it multiplies during the course of multiplication of the bacterial germ plasm (parasitism on the genetic level). The prophage behaves somewhat like a bacterial gene and is carried over to the daughter cells upon cell division. It retains its own characteristics, though, and in particular its capacity to break free of the bacterial genome under the influence of inducing factors (ultraviolet rays, X-rays, various chemicals) or to even develop spontaneously into pathogenic phage particles (vegetative phase) and to bring about lysis of the host cell. Upon completion of lysis infectious phage particles are liberated, infecting receptive bacteria and they can lead to the production of a new lysogenic system. Induction is not possible, however, in all lysogenic bacteria strains.

The prophage gives lysogenic bacteria immunity to the virulent form of the homologous phage and its mutants. These as a rule cannot reproduce themselves in lysogenic bacteria. This has been referred to as “intolerance of related phages on the prophage level.” In rare cases, though, the infecting phage takes the place of the original prophages. Genetic recombinations can also occur. The bacterium cell loses its immunity upon induction. It can be superinfected with virulent mutants of the homologous phage during the vegetative phase. Usually lysogenic bacteria do not have any immunity to unrelated phages, but there are exceptions here, too.[74]

Striking parallels exist between Erich Traub’s writing on these “new lysogenic systems” and the biology of Lyme disease spirochetes. Many decades later, published research reveals that Borrelia burgdorferi carries a family of inducible prophages through the cp32 plasmids that encode critical surface proteins like Erp, OspE, OspF, and Rev families essential for mammalian host invasion, immune evasion, and persistence.[75] Were these the qualities he configured to assist in giving the spirochete broad-spectrum host infectivity and a nice defense system to use against all the new hosts? These prophages can be induced to produce phage particles, facilitate horizontal gene transfer and rapid adaptation.[76]

The presence of this sophisticated system present in the Lyme clade and not Borrelia anserina is consistent with the kind of genetic remodeling Traub was particularly knowledgeable about during his time at Insel Riems.[77] It would indicate that during the adaptation of an avian spirochete, formerly used to birds and soft-bodied Argas ticks, suddenly adapted to hard-bodied Ixodes ticks and hundreds of new animal hosts and reservoirs, prophage elements would have been involved in the bioengineering to create a layered immune evasion and the host-switching capabilities so characteristic of the Lyme Borreliosis clade.

By 1939, when Erich Traub had his protégé Werner Schäfer retrieve strains of Borrelia anserina (then called Spirochaeta gallinarum) from Rockefeller-funded psychiatrist Franz Jahnel,[78] there was already growing demand to remodel Borrelia anserina to be neurotropic and adapted to new animals in order to serve as a better animal model of syphilis, as Jahnel already tried adapting it to numerous species of animals with minimal to no success.[79] Formerly, Borrelia anserina did not invade the central nervous system like the other Relapsing Fever Borrelia, it was unique in this respect.[80]

But Erich Traub and his Insel Riems colleagues had a special talent for this kind of work, as they had changed Foot-and-Mouth Disease Virus (FMD) to go from causing blisters on livestock and guinea pigs to attack the central nervous system by creating a neurotropic mouse-adapted variant that produced a completely different disease than the clinical Foot-and-Mouth Disease by 1938 when Traub was visiting the lab during his trips back to Germany from the Rockefeller Institute.[81] This acted and produced a disease more like polio and they called it mouse polio and were heavily involved in this line of work when Traub became Vice President of Insel Riems.[82] He was clearly doing the same thing to FMD and creating an animal model for the study of polio.

Shortly before Traub went to Insel Riems, however, in 1941 he was actively working with the highly neurotropic viruses such as porcine encephalomyelitis virus (Teschen Disease) and Borna Disease Virus, because in his paper that year experimenting with creating a vaccine for porcine encephalomyelitis, he noted he was actively conducting experiments with Borna Disease Virus.[83] Borna Disease Virus, like Lymphocytic Choriomeningitis Virus (LCM), has a very wide host range, it is able to infect a bewildering number of different animals.[84][85] It is also highly neurotropic,[86] and would have been a choice virus to study if his goal was to study broad-spectrum host infectivity determinants for Borrelia anserina to adapt to hundreds of new animals and a new vector.[87]

During World War II, Erich Traub and Werner Schäfer had been studying the effect of FMD Virus to quickly clear from the blood and attack the epithelium, organs, and tissues,[88] and it does this by binding to cell receptors called integrins,[89] which shows comparable mechanisms with mammalian infection for Borrelia burgdorferi targeting similar integrins, and how it clears from the blood by getting into the tissue, and thus they could have identified certain targets through cellular receptors that all mammals share.[90]

Parallels in Lyme Borrelia and Viral Broad-Spectrum Host Infectivity

Interestingly, Borrelia burgdorferi and some of the viruses with broad-spectrum host infectivity like influenza show some parallels in how this is done in three phases. First, they target host cellular receptors that act as evolutionary constants, in other words, cellular components that have remained unchanged for perhaps millions of years in animal evolution. For some viruses, they do this by utilizing surface glycoproteins that bind to alpha-dystroglycan and neurotrophin, conserved receptors that are widely distributed across vertabrate species.[91][92] For Borrelia burgdorferi, it uses pan-host adhesins like DbpA and BBK32 to bind to decorin and fibronectin, which are ancient extracellular matrix proteins found on every vertebrate tissue on Earth.[93]

Second, they create a decoy system or smokescreen to divert the immune response. For some viruses, they initiate high replication velocity generating a vast swarm of viral mutants known as quasispecies to flood the system of the host by presenting an overwhelming, ever-shifting array of antigenic variants that overwhelm the host’s antibody response.[94] For Borrelia burgdorferi, since they cannot produce a rapid quasispecies cloud, they create a similar mist of diverse antigenic stimuli by shedding a vast array of proteins in what is called blebbing, where its main chromosome directs the shedding of many thousands of hollow outer membrane vesicles (blebs) coated in plasma-derived proteins which act as the perfect decoys absorbing the host’s antibody response and complement attacks.[95][96]

In the third phase, during an ecological shock or jump across highly diverse ecosystems and new hosts, both Borrelia burgdorferi and viruses like Influenza utilize a highly fragmented, segmented genome to execute massive genetic leaps in a condensed timeframe. Though the two target and execute a comparable outcome, their mechanisms for how this is done are somewhat different. Influenza A, for example, possess a segmented genome consisting of 8 distinct RNA strands, where if two different strains infect the same cell inside a host like a bird or pig, the segments physically tangle and swap entire chunks of data in a process called reassortment or antigenic shift which allows the virus to rapidly gain a completely new host tropism without waiting on slow mutations.[97] Borrelia burgdorferi also possess a highly fragmented and segmented genome, carrying a main linear chromosome surrounded by over 20 linear and circular plasmids, and when multiple strains co-infect a single host or tick, which is commonly seen in field samples, they utilize inducible prophages like φBB-1 to physically package and swap whole functional plasmids and cassette assemblies to complete the adaptation process.[98][99]

Unprecedented Evolutionary Dynamics Never Studied in Depth

According to my reconstruction, the weaponization of Borrelia certainly involved extraordinary manmade laboratory bioengineering advantages, giving it the tools it needed to survive and thrive in hundreds of new host immune system types it wasn’t able to infect before. And it wasn’t until it was released into the ecosystems far and wide on different continents during the biological arms race that it underwent rapid unprecedented evolution and divergence as it was subject to an evolutionary crisis, evolved, and adapted to the many hundreds of new host immune systems in a very short timeframe.[100] The spirochete then diversified and took to certain mammals each particular species favored most, but certainly had the capability to infect diverse animals. It was given enough of a fighting chance with some key advantages by the new plasmidome, the mix of co-infections it was growing with, and their ability to induce immunological tolerance in many new hosts. After it was able to overcome the immune systems of each animal and cause immune tolerance with the myriads of other co-infecting agents it invaded with, there would be room for unprecedented rapid evolution made.

Once the rapid unprecedented evolution occurred, it would relax back to a far slower mutation rate and remain fairly conserved between the different genospecies within the Lyme clade, mirroring the estimated mutation rates more commonly seen today,[101] though these are far from reliable estimates since sequencing wild strains using shotgun sequencing is more or less insufficient due to its inherent limitations and the problem of mixed DNA from multiple sources.[102] Once it was used to the various new ecosystems and hosts it had no need to continue such rapid evolution as it had done in its early stages. This would also explain why today’s Lyme Borreliosis clade does not utilize much horizontal gene transfer from other sources other than its own genus, because it has no need for it, it is already well-adapted and thrives, therefore it will conserve itself to maintain that status.

No scientific paper exists that has ever studied such unusual dynamics detailed in my reconstruction of Traub’s bioweaponeering activities during the Second World War at Insel Riems. There have been papers published showing that host immune responses can accelerate pathogen evolution.[103] There have been papers and articles published noting rapid mutation rates in the immunosuppressed.[104] They have studied to a very limited degree accelerated mutation rates in the immune tolerant especially with the use of bats,[105] but they have never studied a dynamic precisely like this where all factors converge across multiple ecosystems within the span of years, though they have noted the possibility that different ecosystems can bring evolutionary changes to living organisms like Borrelia.[106]

Clarification to First Article About the Lyme Clade and Borrelia anserina

To address something in my last paper, Clarification on the Lyme Borreliosis Clade and its relationship to Borrelia anserina, I never stated that any of the factors highlighted in that article, each on their own, like Horizontal Gene Transfer, acquiring antibiotic resistance, or mixing it with multiple infections in a crowded environment, explained the ~25% divergence between Borrelia anserina and the Lyme clade of Borrelia, as Henjin was trying to imply in responding to the article. He was attacking each element on its own as though I was implying each thing on its own could singularly have caused the dramatic shift and that’s not what I was implying. I was explaining that there certainly were many factors that could drive the ~4% divergence in the 16S rRNA gene between them since it is considered the most stable and conserved gene in any given bacteria. I was suggesting that all the factors I listed in toto likely contributed to the ~4% divergence in the 16S rRNA, but then we need to factor into this the ecological shock of multiple new ecosystems, and this would also add further distance at that gene, and would especially account for the larger ~25% divergence.

The cited ~4% divergence between Borrelia anserina and Borrelia burgdorferi is not much of a jump though, because even within Borrelia burgdorferi sensu lato it can vary by roughly ~2%, but then he erroneously claims that if Lyme came from Borrelia anserina it should be 99.99% similar to Borrelia anserina and this is totally undermined by his own graph showing considerable variation in that species. And besides, how could they possibly be that similar currently with all the upgraded system capabilities that Borrelia burgdorferi has that Borrelia anserina didn’t have, being that Borrelia anserina is a simplified, stripped down version of Borrelia burgdorferi? The main chromosome would change in Borrelia burgdorferi since it has to regulate so many new systems in its dynamic capabilities so characteristic of the Lyme clade.

Ecological Dynamics Drive the Evolutionary Divergence

The sophisticated bioengineering techniques and the resulting ecological dynamics I am laying out would demand the spirochete to undergo rapid unprecedented evolution that would certainly affect its main chromosome in order to drive the vast new plasmidome and other regulatory factors it would have been given for its new life.[108] We are talking about it evolving to use an entirely new set of foundational regulations to master the control and expression of a bewildering array of new plasmids and tactics to use against the immune systems of hundreds of new hosts and a new vector across different continents, climates, and ecosystems that Borrelia anserina did not utilize.[109][110] It would have to be able to quickly adjust core regulatory networks, stress-response systems, metabolic flexibility, DNA repair,[111][112] morphological plasticity (blebbing and cyst formation),[113][114] in order to survive the selection pressure stress and sudden change to so many new hosts, who all have different immune systems, more or less hostile to the new spirochete being challenged. In fact, I would argue that such a big leap in evolution would be exactly what one would expect if the spirochete was to survive, adapt, evolve, and thrive under such conditions.[115] Anything less might result in its extinction.[116]

I’m sure it will be argued that adapting it to so many new species at once would be implausible, but not really, especially if the toxic group of polymicrobial co-infections it was growing with was able to create intense synergy and an induce immune tolerance-like state in many of the new hosts.[117][118] Not to mention the fact that Traub had expertise in viruses that could infect a wide range of animals, and he could have certainly identified factors responsible for broad-spectrum host infectivity.

Once thrust into an environment of hundreds of new hosts in diverse ecosystems in a very short timeframe, the mutation rates and genetic exchanges would be greatly accelerated to adjust itself to the new situation, it would rapidly evolve to rise to the challenge of each new immune system and it would fight back to induce immune tolerance in many of these hosts, where it could then thrive and rapidly mutate further. In these early stages it would be operating under completely different rules than how it acts today in a well-adapted situation, and it could certainly utilize gene transfer in this type of crisis situation. It would also be subject to genetic exchange to the specific microbiome of each ecosystem which could change the spirochetes between different climates and ecosystems considerably. [119][120]

And again, once it rose to the challenge and made the necessary changes it needed and evolved, it would then start to relax its mutation rate to something much slower or even into a purifying phase, since it’s only going to rapidly evolve until it has fully adapted itself.[121] Nature only evolves when it absolutely must. Henjin at one point tried presenting data from the 16S rRNA gene of Borrelia burgdorferi comparing it to Borrelia anserina, without a timeframe, showing Borrelia burgdorferi to be under negative selection pressure, but this is not a valid argument, because this would have been long after the fact when it has already made the necessary changes and reverted to a purifying phase where Borrelia burgdorferi is at right now.[122][123]

Likewise, he will probably continue arguing that all of these adaptations would only affect the plasmids, but no, the many challenges, selection pressures, and changes it would demand, to be able to use the bewildering array of new plasmids and multiple other regulatory factors would demand it to change its core main chromosome to regulate all of these new tactics and capabilities.[124][125] Borrelia anserina did not have these capabilities before, it needed to be fully upgraded and redesigned from the inside.

Once the jump was made and evolved into the Lyme clade it would cluster much closer together and the different continents it was released on could change it dramatically in the beginning, even into new genospecies in a relatively short time, this mirrors what we see, the different continents having certain genospecies within the Lyme clade and all of them cluster closely together to one another.[126] Its survival would be helped especially if it was combining with other genetic material from other species of Borrelia already in these animals.[127]

The tick-borne cocktail of pathogens could have provided a synergistic environment that allowed it to assimilate foreign material and additional plasmids.[128] The ability of this Russian-doll cocktail of co-infecting agents to induce immune tolerance (immunosuppression and persistent infection) in many of the hosts then allows the mutation rate to jump dramatically beyond anything seen in standard laboratory evolution experiments or natural host cycles in which it is already used to and adapted to. [129] Once it’s able to survive and thrive, the selection pressure is going to disappear because it’s made all the necessary changes it needed and it happened very quickly and from that point forward it starts purifying what it doesn’t need.[130]

Ecological Selection Pressure and Immune Tolerance

It may at first glance seem contradictory that I’m saying the remodeled spirochete is under intense selection pressure by all the different immune systems yet its inducing immune tolerance, but I should explain further, at first in the host the immune system interaction creates intense pressure on the spirochete but once it starts utilizing the new plasmidome properly along with the mix of co-infecting agents which create a synergistic effect, it soon overcomes the host defenses and induces immune tolerance and quickly overtakes the host to thrive. Again, the main chromosome would certainly be involved in expressing and regulating these new plasmids, even if much of the immune evasion and tissue tropism happens through the plasmids directly.[131] The main chromosome carries core housekeeping genes and stress-response genes, so under strong selection pressure the main chromosome could change considerably under such unusual circumstances, which brings more or less an ecological shock demanding the spirochete to adapt or be extinguished from existence.[132]

Changes to its main chromosome would include modifying the regulation of blebbing (shedding its outer surface proteins), a stress response like a Star Wars defense system to overcome and evade the immune system.[133] Borrelia anserina does not have this capability,[134] therefore structural upgrades would have been necessary for the massive change to so many new hosts with additional capabilities like blebbing and using a much more complex plasmidome.

The chromosome controls multiple factors of plasmid activity under different cycles of infection.[135] It would regulate the formation of cyst-forms, this takes morphological plasticity under attack and requires coordinated changes in cell-wall synthesis, membrane dynamics, and stress-response pathways.[136] Many of these are encoded in the chromosome even if the plasmids are doing most of the heavy lifting, the chromosome is what orders them into action and demands what needs to be done.[137] The general persistence mechanisms are also somewhat regulated from the chromosome, even though mainly driven from its plasmid expression, and when genes involved in DNA repair, metabolic flexibility, oxidative stress resistance, and global gene regulation are used it would need core tuning to its chromosome to adjust and survive the pressure from so many new hosts.[138]

Manmade Biowarfare Activities Accelerating Unprecedented Evolution

Manmade biodefense and biowarfare activities have been with us for well over a century and beyond, and the releasing of a bioengineered bacteria with a mix of co-infections with harmful capabilities across diverse ecosystems across the globe would be considered highly unethical so no published research would openly admit these events have occurred and would not openly study them in that light. And even releasing so-called harmless microbes in simulant tests has been controversial and often kept secret.[139] There would be severe backlash admitting such an experiment and you’d be hard pressed to find it, as books documenting such scandals have already made things unpleasant for the U.S. Government from tests in the 1950s.[140]

Borrelia anserina thrived in a very stable, narrow two-host cycle in soft-bodied Argas ticks and birds with only a minimal plasmidome.[141] The Lyme clade on the other hand displays one of the most dynamic plasmid systems known in bacteria, as it is constantly reshuffling plasmids and their expression as it moves back and forth between hard-bodied ticks and hundreds of vertebrate hosts.[142]

Borrelia burgdorferi possesses a multi-layered, structured regulatory system (RpoS as a broad patrol, Rrp1/c-di-GMP as a central signaling hub, and CyaB, an enzyme that produces cyclic adenosine monophosphate (cAMP), and this is important for virulence factors and successful mammalian infection.[143] It shows a dynamic variable major protein-like single action expression site (vlsE) system capable of rapid, continuous diversification under immune pressure.[144]

Borrelia anserina did not have these far more sophisticated vlsE-like antigenic variation mechanisms that the Lyme clade possesses. [145] This has gained a highly changeable, recombination-prone vlsE cassette as a major upgrade for surviving diverse mammalian immune systems.[146] And if that weren’t enough it can also utilize dormant forms and change its physical state to assume spheroblasts, as demonstrated in paper “Formation and Cultivation of Borrelia burgdorferi Spheroblast-L-Form Variants.”[147]

It can remain dormant in these forms and seem non-infectious, but spirochetes assuming these cyst-forms or spheroblasts can rapidly change back into active motile spirochetes rather quickly, as was shown in the paper “Transformation of Cystic Forms of Borrelia burgdorferi to Normal, Mobile Spirochetes”:

When rabbit serum or BSK was added to [RPMI-1640 Select-Amine (RPMI) (Life Technologies); RPMI is a defined medium containing glucose, vitamins, and all 20 of the protein amino acids] containing 48h serum-starved cells, the cysts opened within 10 [seconds] to yield intact, but non-motile spirochaete cells. […] Cells began to regain motility 12–15 [hours] after emerging from the cysts.[148]

This biological weapon or Russian-doll cocktail of disease agents and weaponized Lyme disease was given supreme fitness by the malefic talent of Erich Traub. It carries his entire life work within its evolution. Erich Traub was known for mixing pathogens together in a cocktail of infectious disease agents. That’s precisely how he adapted Foot-and-Mouth Disease Virus to chicken eggs when no one had succeeded prior attempts:

Although many attempts were made, the virus of FMD was not successfully propagated in this manner until the work of Dr. Traub of Germany was uncovered soon after World War II. He had succeeded in cultivating FMD virus by mixing 10 strains of the virus and inoculating them into embryonating eggs. Although the strain of virus that actually was propagated was not known. Dr. Traub ‘s work showed adaptation of the egg to propagation. His results could not be repeated until recently when the English workers confirmed his observations.[149]

We know the Germans were looking to adapt Borrelia anserina to the central nervous system to become an animal model for the study of syphilis,[150] and we know they were hoping to adapt it to mice and other animals.[151] Traub was able to do exactly this to the FMD Virus.[152] We know Erich Traub was looking to induce the state of immune tolerance, which he had first discovered in 1936 by intercerebral inoculations of foreign protein into a mouse brain and reactivating dormant LCM Virus from within the mouse starting an epidemic from scratch.[153]

Not only did he hold the expertise to adapt Borrelia anserina to the Central Nervous System and brain, and not only was he knowledgeable about how the mix of co-infections could induce the immune tolerance phenomenon he spent his life studying.[154] He also had expertise on adapting agents to new hosts,[155] and held expertise on viral agents with broad-spectrum host infectivity.[156][157][158] Likewise, he held expertise in using mollicutes like Mycoplasma mycoides as gene shuttles between the different co-infecting agents along with viruses to create an ultra-synergistic environment for rapid adaptation.[159] Furthermore, he had expertise on how viruses could be used to create new lysogenic systems in bacteria, as he had hinted this expertise in his papers on Eastern Equine Encephalomyelitis Virus (EEE).[160]

Reinforcing the Consensus: Ai and its Barriers to Honest Answers

Henjin can try to explain this away a thousand ways to Sunday with his multiple Ai companions but we’re still left with the fact that no paper or study has ever meaningfully studied these complex ecological variables and evolutionary dynamics laid out in my reconstruction. Ai can certainly be helpful for certain things, but clearly many are starting to become too dependent on it dictating to us what reality is or isn’t, and all of the Ai LLMs are designed to mimic human behavior in communication, and they will always give an establishment consensus answer by proxy, and sometimes they will even play to your bias, that’s how they were designed.

Everyone is aware by now how often Ai lies and offers hallucinatory explainations on many occasions. It is no more reliable than a human is, and Henjin gets all his answers and arguments from Artificial Intelligence models, it tells him what to say, or he just copies and pastes its answers like he did responding to my last few articles and he has it make him colorful graphs to try and debunk whatever he doesn’t agree with. Yet if you talk to any Ai models long enough and put forward enough evidence like that which I have accumulated over many years, they end up changing their position. In one conversation with Grok that took Henjin’s position at first, it soon changed its mind and thinks my reconstruction is the most plausible explanation.

I’m sure Henjin’s LLM models will tell him the opposite, that his argument is the stronger one, and that’s why folks, we can’t rely on Ai slop to mediate for us. It does all the same things humans do because it’s meant to mimic our behavior, so it picks sides, and reverts to group think consensus views. Even if it gave 100% honest answers in all instances, It could not know all the possibilities that exist in a situation like this because no scientific papers or laboratory research has ever replicated and studied such a dynamic of factors all converging together like this, such as: What happens to a microbe when it goes from being used to one or two simple hosts for perhaps millions of years, and suddenly through manmade adaptation in an unusual, crowded Russian-doll cocktail of polymicrobial superinfection and viral assistance it is given entirely new characteristsics on every level, induces broad-spectrum host infectivity and is exposed to multiple ecosystems with hundreds of new hosts on different continents, all with unique immune systems (different complement systems, antimicrobial peptides, tissue environments, body temperatures, etc.)?

Its the dogma of mainstream establishment science and evolutionary theory that always has to assume that changes to microbes must have occured hundreds of thousands to millions of years ago, yet the same establishment contradicts itself by maintaining that so many new diseases and changes to the ecosystem are the result of recent manmade climate change, yet they never consider that major changes to microbes could have been recent events because they have to cater to the biodefense industry’s secretive National Security banner and to this long-held slow evolution paradigm. Yet they admit many of the changes that occur to microbes millions of years ago like host switching are rapid events that do not happen slowly, there’s no way they could know whether it was far in the distant past or recent, meanwhile Laboratory adaptation has been going on for well over a Century, and since establishment science and biodefense are very often intermixed, they are sure not to imply any changes are the result of manmade biowarfare activity and human driven adaptation which has been rife in the last Century, but they sure love to milk the tax dollars of every American to protect against just that.

The ~25% Divergence: A Signature of Ecological Shock and Evolution

The cited ~25% divergence between Borrelia anserina and Borrelia burgdorferi would be entirely consistent with what we would expect to see. While this number could be somewhat inaccurate, a big jump would still be expected, as the agent was released on many different continents by different superpowers in the biological arms race, each with their own unique ecosystem. This could result in new genospecies and variants that would cluster closely together,[161] much like we see with the Lyme clade. All of this could occur in a very short time and once it had created the necessary changes through rapid evolution it would then relax back into a slower purified genetic state, which seems to have already occurred.

The fact that the Lyme clade is suddenly now the most abundant form of Borrelia on the globe is also explainable in this light, and it explains why not one sample of the Lyme clade or a spirochete matching the morphology of Borrelia anserina in other mammals was found before World War II, because it had not been remodeled yet and given broad-spectrum host infectivity.

Studies claiming it was found in ancient mummies say in the studies they don’t even know what bacteria it actually is, yet they continue to push it as fact that the mummy had Lyme disease.[162] Other studies claiming it was in ticks and mouse samples from the 1800s never tested for the flagellin gene sequences but only for OspA,[163][164] which is extracellular surface proteins that change regularly, so these are not enough to speak to a Borrelia burgdorferi infection, but yet again, they continued pushing it as fact. It’s telling that they chose not to test for the flagellin gene sequence in these older samples,[165] but did so for the ticks tested in the late 1940s and early 1950s that actually back up my reconstruction.[166]

The rise of Lyme disease was a very recent event. Even in papers discussing the sudden explosion of the Lyme borreliosis clade call it a “recent emergence,” even though they try to backdate it thousands of years as though it was from ice sheets thawing,[167] the fact that they refer to it as a “recent emergence” is contrary language to a slow, steady natural evolution. Furthermore, this is often contradicted by the scientific establishment trying to blame it on climate change which is mostly from the last century.[168] But we’ve already shown that despite “the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.”[169]

The big gap between Borrelia anserina and the Lyme clade is explainable by the massive bioengineering given to the spirochete from Traub’s many lines of expertise all converging into one locus and released on diverse ecosystems on every continent. It was in this fitness test being challenged with an unpredictable set of variables and new host defenses one after the other in an ecological shock and evolutionary crisis. Traub gave it enough of a fighting chance not only with the cocktail of co-infecting agents he mixed it with but also with the viruses and mycoplasma he used to help the bacteria adapt to the challenging new situation.

It is in these unusual areas of expertise and methods of genetic engineering and remodeling that Erich Traub excelled in to create this new class of biological weapons agents, and the weaponized spirochete actually shows every aspect of Traub’s life work converging together; his deep knowledge of viral-bacterial interactions and lysogenic systems,[170] his expertise in the art of adaptation getting disease agents to infect new species they didn’t infect beforehand,[171] combining biological agents in mixed infections that induce immune tolerance,[172] a condition he discovered and studied for his entire life, and finally, adapting biological agents to the central nervous system and making them more neurotropic.[173]

The pattern of such a striking morphological match Between Borrelia anserina and Borrelia burgdorferi,[174] sharing flagellar epitopes,[175] and infecting the same hosts in birds,[176] fits the rapid manmade bioengineering scenario perfectly. It was given the helping hand of Erich Traub and his Insel Riems crew and subjected to intense, high-pressure artificial conditions with multiple competing co-infections and immune tolerant hosts which would drive the mutation rates up excessively and force the big leap to the Lyme clade while preserving the core structural features in morphology, flagellar apparatus, and basic motility that were advantageous. This would mirror today’s picture, a cluster of Borrelia that have similar morphology and the basic architecture of Borrelia anserina with fully upgraded components and now thrives in hundreds of new hosts and diverse ecosystems, with an entirely new plasmid system, varying tropisms and disease-causing abilities.

This may also explain why Borrelia anserina has nearly dropped off the research map and become a forgotten disease by modern science, because its re-engineered form (the Lyme clade) has greatly outpaced it and created an immune tolerant-like state in which the birds that normally would have been killed by the fatal avian spirochetosis are now immune tolerant carriers of Borrelia anserina and Borrelia burgdorferi.

With all the factors presented here, this is all entirely uncharted territory for science and the study of evolution. However, enough evidence exists to show a compelling case that explains all of the many anomalies surrounding Lyme disease as a recent event from manmade conditions in the biological warfare race. It also shows just how skillful Erich Traub was in his biological weapons work, and no doubt why his technical assistant Anne-Lise Bürger’s approval to come to the United States noted that there were no top rate scientists in America that could match or replace the level of skill and expertise that she and Erich Traub held.[177]

This also shows for the record that Willy Burgdorfer was not the man with the expertise or skill to have weaponized Lyme disease spirochetes, he did not have even a fraction of the expertise that Erich Traub held and it could be argued that Traub might have been the only one on Earth at that time skilled and original enough to put this superweapon together. I think Willy and his American biodefense colleagues may have further spread these ticks unwittingly after Traub returned to West Germany, so it does not necessarily contradict what was in Kris Newby’s Bitten: The Secret History of Lyme Disease and Biological Weapons, but the biological superweapon has Erich Traub’s signature all over it.

My work is not debunked by any means, my position stands. The 25% divergence is not a marker of impossibilities for the Borrelia spirochetes, rather it is the signature of its survival under an intense and unprecedented time of a manmade directed evolution.

Sources

[1] OpenVAET. (2024b, July 27). Dunning-Kruger Illustrated, ASMR explained & bad non-official Czech data. Dunning-Kruger Illustrated, ASMR Explained & Bad Non-Official Czech Data.

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Dunning-Kruger Illustrated, ASMR Explained & Bad Non-Official Czech Data

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[2] Koblentz, Gregory D. “The Danger of Disinformation: Understanding Propaganda Campaigns Against Biological Facilities.” Nonproliferation Review, vol. 27, no. 4-6, 2020, pp. 419–437, doi:10.1080/10736700.2020.1866418.

[3] Telford, Sam. “No, Lyme Disease Is Not an Escaped Military Bioweapon, despite What Conspiracy Theorists Say.” The Washington Post, WP Company, 11 Aug. 2019, https:// www.washingtonpost.com/health/no-lyme-diease-is-not-an-escaped-military-bioweap on- despite-what-conspiracy-theorists-say/2019/08/09/5bbd85fa-afe4-11e9-8e77-03b30b c29f64_ story.html

[4] Henjin. (2026, March 29). Did Borrelia anserina become Borrelia burgdorferi? Response by Grok. Sars2.net. Retreived from: https://sars2.net/lyme2.html#Did_Borrelia_anserina_become_Borrelia_burgdorferi

[5] Finnegan, A. W. (2023). The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. Trine Day.

[6] Trevisan, Giusto et al. “Borreliae Part 2: Borrelia Relapsing Fever Group and Unclassified Borrelia.” Biology vol. 10,11 1117. 29 Oct. 2021, doi:10.3390/biology10111117

[7] Trevisan, Giusto et al. “Borreliae Part 1: Borrelia Lyme Group and Echidna-Reptile Group.” Biology vol. 10,10 1036. 12 Oct. 2021, doi:10.3390/biology10101036

[8] Finnegan, A. W. (2023). The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. Trine Day.

[9] Marconi, R T et al. “Identification of novel insertion elements, restriction fragment length polymorphism patterns, and discontinuous 23S rRNA in Lyme disease spirochetes: phylogenetic analyses of rRNA genes and their intergenic spacers in Borrelia japonica sp. nov. and genomic group 21038 (Borrelia andersonii sp. nov.) isolates.” Journal of clinical microbiology vol. 33,9 (1995): 2427-34. doi:10.1128/jcm.33.9.2427-2434.1995

[10] Hovind-Hougen, K. “A Morphological Characterization of Borrelia anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[11] Stevenson, Brian. “The Lyme disease spirochete, Borrelia burgdorferi, as a model vector-borne pathogen: insights on regulation of gene and protein expression.” Current opinion in microbiology vol. 74 (2023): 102332. doi:10.1016/j.mib.2023.102332

[12] Hovind-Hougen, K. “A Morphological Characterization of Borrelia Anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[13] Walker, R. L., Greene, R. T., Nicholson, W. L. & Levine, 1. F. Shared flagellar epitopes of Borrelia burgdorjeri and Borrelia anserina. Vet Microbiol. 19, 361-371. (1989)

[14] Becker, DJ, Han, BA. The macroecology and evolution of avian competence for Borrelia burgdorferi. Global Ecol Biogeogr. 2021; 00: 1– 15. https://doi.org/10.1111/geb.13256.

[15] Bózsik, András Pál et al. “Presence of Borrelia Spirochetes in White Stork (Ciconia ciconia), White-Tailed Eagle (Haliaeetus albicilla), and Eastern Imperial Eagle (Aquila heliaca): Hospitalized in a Wild Bird Hospital and Sanctuary (Hortobágy, Hungary).” Animals : an open access journal from MDPI vol. 14,24 3553. 10 Dec. 2024, doi:10.3390/ani14243553

[16] Hillis, David M., et al. “Review: Morphological Phylogenetics in the Genomic Age.” Current Biology, vol. 25, no. 19, 2015, pp. R880–R888, doi:10.1016/j.cub.2015.07.034.

[17] Hovind-Hougen, K. “A Morphological Characterization of Borrelia Anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[18] Casjens, Sherwood R., et al. “Inter- and Intra-Specific Pan-Genomes of Borrelia burgdorferi Sensu Lato.” BMC Genomics, vol. 14, no. 693, 2013, pp. 1–24, doi:10.1186/1471-2164-14-693.

[19] Schäfer, W. (1939). Fortführung von Spirochaeta gallinarum-Stämmen von Eipassagen. [The Maintenance of Spirochaeta gallinarum by Passage in Fowl Embryos.] Vet. Bull., 11, 220.

[20] Hovind-Hougen, K. “A Morphological Characterization of Borrelia anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[21] Bózsik, András Pál et al. “Presence of Borrelia Spirochetes in White Stork (Ciconia ciconia), White-Tailed Eagle (Haliaeetus albicilla), and Eastern Imperial Eagle (Aquila heliaca): Hospitalized in a Wild Bird Hospital and Sanctuary (Hortobágy, Hungary).” Animals : an open access journal from MDPI vol. 14,24 3553. 10 Dec. 2024, doi:10.3390/ani14243553

[22] Koutantou, Myrto et al. “Prevalence of Lyme Disease and Relapsing Fever Borrelia spp. in Vectors, Animals, and Humans within a One Health Approach in Mediterranean Countries.” Pathogens (Basel, Switzerland) vol. 13,6 512. 17 Jun. 2024, doi:10.3390/pathogens13060512

[23] Hovind-Hougen, K. “A Morphological Characterization of Borrelia anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[24] Steiner, G. “Acute plaques in multiple sclerosis, their pathogenetic significance and the role of spirochetes as etiological factor.” Journal of neuropathology and experimental neurology vol. 11,4 (1952): 343-72. doi:10.1097/00005072-195210000-00001

[25] Harding, H B et al. “Is multiple sclerosis caused by Spirochaeta myelophthora (Steiner)?.” Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) vol. 102 (1959): 217-20. doi:10.3181/00379727-102-25197

[26] Ichelson, R. “Cultivation of spirochaetes from spinal fluids of multiple sclerosis cases and negative controls.” Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) vol. 95,1 (1957): 57-8. doi:10.3181/00379727-95-23117

[27] Loftus, John. Americas Nazi Secret: an Insiders History of How the United States Department of Justice Obstructed Congress by: Blocking Congressional Investigations into Famous American Families Who Funded Hitler, Stalin and Arab Terrorists ; Lying to Congress, the GAO, and the CIA about the Postwar Immigration of Eastern European Nazi War Criminals to the US ; and Concealing from the 9/11 Investigators the Role of the Arab Nazi War Criminals in Recruiting Modern Middle Eastern Terrorist Groups. TrineDay LLC, 2011.

[28] Margos, Gabriele et al. “The genus Borrelia reloaded.” PloS one vol. 13,12 e0208432. 26 Dec. 2018, doi:10.1371/journal.pone.0208432

[29] Ivanova, Larisa B. et al. “Borrelia chilensis, a new member of the Borrelia burgdorferi sensu lato complex that extends the range of this genospecies in the Southern Hemisphere.” Environmental microbiology vol. 16,4 (2014): 1069-80. doi:10.1111/1462-2920.12310

[29a] Margos, Gabriele, et al. “Borrelia bavariensis: Vector Switch, Niche Invasion, and Geographical Spread of a Tick-Borne Bacterial Parasite.” Frontiers in Ecology and Evolution, vol. 7, article 401, 2019, https://doi.org/10.3389/fevo.2019.00401

[29b] Bacigalupe, Rodrigo et al. “A multihost bacterial pathogen overcomes continuous population bottlenecks to adapt to new host species.” Science advances vol. 5,11 eaax0063. 27 Nov. 2019, doi:10.1126/sciadv.aax0063

[29c] Yebra, Gonzalo et al. “Radical genome remodelling accompanied the emergence of a novel host-restricted bacterial pathogen.” PLoS pathogens vol. 17,5 e1009606. 20 May. 2021, doi:10.1371/journal.ppat.1009606

[30] Alhamadn, Mohammed AM. “The Association Between Climate Change and Lyme Disease Incidence in Northern European Countries by the Baltic and North Seas: An Ecological Time-Series Study.” medRxiv, 27 Aug. 2025, doi:10.1101/2025.08.24.25334298v1.

[31] Christopher, G. et al. Biological warfare. A historical perspective. JAMA, 278(5), 412–417. (1997)

[32] Humphrey, Parris T. et al. “Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis.” Evolution; international journal of organic evolution vol. 64,9 (2010): 2653-63. doi:10.1111/j.1558-5646.2010.01001.x

[33] Rogers, Andrew Jackson. “A Study of the Ixodid Ticks of Northern Florida, Including the Biology and Life History of Ixodes Scapularis Say (Ixodidae: Acarina).” University of Maryland & University of Florida, University of Maryland, 1953. Retrieved from: https://drum.lib.umd.edu/bitstream/handle/1903/16865/931201.pdf

[34] Burgdorfer, Willy, et al. “Lyme Disease—A Tick-Borne Spirochetosis?” Science, vol. 216, no. 4552, 1982, pp. 1317–1319, doi:10.1126/science.7043737.

[35] Hamer, Sarah A et al. “Diverse Borrelia burgdorferi strains in a bird-tick cryptic cycle.” Applied and environmental microbiology vol. 77,6 (2011): 1999-2007. doi:10.1128/AEM.02479-10

[36] Arthur, Don R. “Studies on Exotic Ixodes Ticks (Ixodoidea, Ixodidae) from United States Navy and Army Activities.” The Journal of Parasitology, vol. 43, no. 6, 1957, pp. 681–694, doi:10.2307/3286566

[37] Chrisman, Brianna et al. “The human “contaminome”: bacterial, viral, and computational contamination in whole genome sequences from 1000 families.” Scientific reports vol. 12,1 9863. 14 Jun. 2022, doi:10.1038/s41598-022-13269-z

[38] Carpi, G., Walter, K. S., Bent, S. J., Hoen, A. G., Diuk-Wasser, M., & Caccone, A. (2015). Whole genome capture of vector-borne pathogens from mixed DNA samples: a case study of Borrelia burgdorferi. BMC Genomics, 16(1). doi:10.1186/s12864-015-1634-x

[39] Hepner, S., et al. “Telomere-to-Telomere Assembly Detects Genomic Diversity in Borrelia burgdorferi.” Cell Reports, vol. 44, no. 11, 2025, e101247, doi:10.1016/j.celrep.2025.101247.

[40] Sequencing microbes with greater genomic context | the scientist. The Scientist. (n.d.). https://www.the-scientist.com/sequencing-microbes-with-greater-genomic-context-74634

[41] Trivedi, P., Wang, N. Host immune responses accelerate pathogen evolution. ISME J 8, 727–731 (2014). https://doi.org/10.1038/ismej.2013.215

[42] Wright, S. (2011, January 28). A new appreciation of the ecology-evolution dynamic. UC Davis. https://www.ucdavis.edu/news/new-appreciation-ecology-evolution-dynamic

[42a] Pei, Anna Y et al. “Diversity of 16S rRNA genes within individual prokaryotic genomes.” Applied and environmental microbiology vol. 76,12 (2010): 3886-97. doi:10.1128/AEM.02953-09

[43] Zhang, Jing-Ren, et al. “Antigenic Variation in Borrelia burgdorferi by Segmental Gene Conversion.” Science, vol. 276, no. 5312, 1997, pp. 571–575.

[44] Livermore, Bryan P., et al. “The Borrelia burgdorferi SOS Response and Its Role in Mutagenesis and Survival under Oxidative and Host-Induced Stress.” Journal of Bacteriology, vol. 198, no. 14, 2016, pp. 1941–1952.

[45] Bruckbauer, H R et al. “Cross-reactive proteins of Borrelia burgdorferi.” European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology vol. 11,3 (1992): 224-32. doi:10.1007/BF02098084

[46] Grąźlewska, Weronika, and Lucyna Holec-Gąsior. “Antibody Cross-Reactivity in Serodiagnosis of Lyme Disease.” Antibodies (Basel, Switzerland) vol. 12,4 63. 5 Oct. 2023, doi:10.3390/antib12040063

[47] Aberer, E et al. “Molecular mimicry and Lyme borreliosis: a shared antigenic determinant between Borrelia burgdorferi and human tissue.” Annals of neurology vol. 26,6 (1989): 732-7. doi:10.1002/ana.410260608

[48] Hinnebusch, J, and A G Barbour. “Linear plasmids of Borrelia burgdorferi have a telomeric structure and sequence similar to those of a eukaryotic virus.” Journal of bacteriology vol. 173,22 (1991): 7233-9. doi:10.1128/jb.173.22.7233-7239.1991

[48a] Casjens, S et al. “Telomeres of the linear chromosomes of Lyme disease spirochaetes: nucleotide sequence and possible exchange with linear plasmid telomeres.” Molecular microbiology vol. 26,3 (1997): 581-96. doi:10.1046/j.1365-2958.1997.6051963.x

[49] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

[50] Popov, Georgi et al. “Tick-Borne Co-Infection in Lyme Disease: Clinical Impact, Diagnostic Challenges, and Therapeutic Perspectives.” Microorganisms vol. 14,2 325. 30 Jan. 2026, doi:10.3390/microorganisms14020325

[51] Beller, K. Herzwasser und sonstige tierische Rickettsiosen [Heartwater and other animal rickettsioses]. Handbuch der Viruskrankheiten (Ed. E. Gildermeister, E. Haagen, O. Waldmann). Vol. 2, Section 7, chapter 3, pp. 606-623. (1939) [Translated to English by A. Finnegan, 2021]

[52] Popov, Georgi et al. “Tick-Borne Co-Infection in Lyme Disease: Clinical Impact, Diagnostic Challenges, and Therapeutic Perspectives.” Microorganisms vol. 14,2 325. 30 Jan. 2026, doi:10.3390/microorganisms14020325

[53] Doucleff, M. (2021, February 05). Extraordinary patient offers surprising clues to origins of coronavirus variants. Retrieved February 20, 2021, from https://www.npr.org/sections/goatsandsoda/2021/02/05/964447070/where-did-the-coronavirus-variants-come-from?

[54] Tanaka, Mark M., et al. “Antigenic Escape Is Accelerated by the Presence of Immunocompromised Hosts.” Proceedings of the Royal Society B: Biological Sciences, vol. 289, no. 1986, 2022, pp. 1–9, doi:10.1098/rspb.2022.1437.

[55] Didelot, Xavier, et al. “Within-Host Evolution of Bacterial Pathogens.” Nature Reviews Microbiology, vol. 14, no. 3, 2016, pp. 150–162, doi:10.1038/nrmicro.2015.13.

[56] Chubbyemu. (2026, March). Syphilis Is Evolving Like Never Before.. In Michigan. Chubbyemu YouTube Channel.

[57] Ebinger, Arnt et al. “Lethal Borna disease virus 1 infections of humans and animals - in-depth molecular epidemiology and phylogeography.” Nature communications vol. 15,1 7908. 10 Sep. 2024, doi:10.1038/s41467-024-52192-x

[58] Schrauwen, Eefje J. A., and Richard A. M. Fouchier. “Zoonotic Potential of Influenza A Viruses: A Comprehensive Overview.” PubMed Central (PMC), vol. 10, no. 9, 2018, pp. 1–18, doi:10.3389/fmicb.2018.00104.

[59] Moraz, Michelle C., et al. “Lymphocytic Choriomeningitis—Emerging Trends of a Neglected Zoonosis.” Microorganisms, vol. 9, no. 5, 2021, e1013, doi:10.3389/fmicb.2021.654215.

[60] Babb, Kelly et al. “Borrelia burgdorferi EbfC, a novel, chromosomally encoded protein, binds specific DNA sequences adjacent to erp loci on the spirochete’s resident cp32 prophages.” Journal of bacteriology vol. 188,12 (2006): 4331-9. doi:10.1128/JB.00005-06

[61] Zhang, Hongming et al. “bdrF2 of Lyme disease spirochetes is coexpressed with a series of cytoplasmic proteins and is produced specifically during early infection.” Journal of bacteriology vol. 187,1 (2005): 175-84. doi:10.1128/JB.187.1.175-184.2005

[62] National Archives. Joint-Intelligence Objectives Agency file on Erich Traub (RG 330). NARS. Joint Intelligence Objectives Agency (JIOA), JIOA Administrative Records. (1949- 54).

[63] Ruska, H: Zur Frage der Potenzierung von Bakteriophagenlösungen durch Zerschäumen [On the question of the potentiation of bacteriophage solutions by foaming]. Kolloid-Zeitschrift 110 (1948), S. 175-177 [paper submitted in 1945, not published until 1948.]

[64] Ruska, H., & C. Menze: Die Größe von Typhusbakteriophagen nach der Filtrationsendpunktbestimmung und dem elektronenmikroskopischen Bild. [The size of typhus bacteriophages after the final filtration point determination and the electron microscopic picture.] Kolloid-Zeitschrift 110 (1948), S. 103-105

[65] Ruska, H., Über die Elementarkörper des Virus der Bronchopneumonie der Maus. [On the elementary bodies of the virus of bronchopneumonia of mice.] Klinische Wochenschrift 23 (1944), S. 121-122

[66] Dinter, Z., Uber eine der Rollkrankheit ähnliche Infektion der weißen Maus Berl. Munch, tierärztl. Wschr, 6, 68-69. (1946)

[67] Ruska, H., & K. Poppe: Elektronenmikroskopische Untersuchungen zur Morphologie der Seiffertschen Mikroorganismen und des Erregers der Lungenseuche des Rindes. [Electron Microscopy Investigations on the morphology of Seiffert’s Microorganism and the causative agent of bovine respiratory disease]. Zeitschrift für Hygiene und Infektionskrankheiten, medizinische Mikrobiologie, Immunologie und Virologie 127 (1947), S. 201-215

[68] Eggers, Christian H et al. “Phage-mediated horizontal gene transfer of both prophage and heterologous DNA by ϕBB-1, a bacteriophage of Borrelia burgdorferi.” Pathogens and disease vol. 74,9 (2016): ftw107. doi:10.1093/femspd/ftw107

[69] Traub, E., Schafer, W. & Schramm, G., Untersuchen uber das Virus der Atypischen Geflugelpest. [Studies of the Virus of Atypical Fowl Plague]. Z. Naturforsch B. 157-167 (1949). [Translated to English by A. Finnegan (2019)]

[70] Traub, E., et al. Untersuchungen über die Stomatitis papulosa des Rinde. [Studies on bovine papular stomatitis] Zeit. Infek. Krank. Hyg. Haus. 56 (2): 85-103. (1940). [Translated to English by A. Finnegan, 2019]

[71] Leitenberg, Milton, et al. The Soviet Biological Weapons Program: a History. Harvard University Press, 2012.

[72] BAYREUTHER, K E, and W R ROMIG. “POLYOMA VIRUS: PRODUCTION IN BACILLUS SUBTILIS.” Science (New York, N.Y.) vol. 146,3645 (1964): 778-9. doi:10.1126/science.146.3645.778

[73] Abel, P., Trautner, T.A. Formation of an animal virus within a bacterium. Zeitschrift für Vererbungslehre 95, 66–72 (1964). https://doi.org/10.1007/BF00898185

[74] Traub, E., Uber die Immunitat der weißen Maus gegenüber dem EEE-Virus. VIII. Mitteilung. Zusammenfassende Diskussion. [On the immunity of the white mouse to the EEE-virus. VIII. Summarizing Discussion]. Z Immun Exp Ther. 122(3):239-58. (1961). [Translated to English by A. Finnegan (2019)]

[75] Stevenson, Brian, and Catherine A Brissette. “Erp and Rev Adhesins of the Lyme Disease Spirochete’s Ubiquitous cp32 Prophages Assist the Bacterium during Vertebrate Infection.” Infection and immunity vol. 91,3 (2023): e0025022. doi:10.1128/iai.00250-22

[76] Casselli, Tami, et al. “Coupled Induction of Prophage and Virulence Factors during Tick Feeding Facilitates Lyme Disease Spirochete Transmission.” Nature Communications, vol. 14, no. 1, 2023, pp. 1–16, doi:10.1038/s41467-023-35897-3.

[77] Finnegan, A. W. (2023). The sleeper agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. Trine Day.

[78] Schäfer, W. (1939). Fortführung von Spirochaeta gallinarum-Stämmen von Eipassagen. [The Maintenance of Spirochaeta gallinarum by Passage in Fowl Embryos.] Vet. Bull., 11, 220.

[79] Jahnel, F., Untersuchungen über die Hühnerspirochätose mit besonderer Berücksichtigung der vergleichenden Pathologie der Spirochätenerkrankungen. Wissenschaftl. Sitzg d. Dtsch. Forschungsanstalt f. Psychiatrie (Kaiser Wilhelm-Institut) München, am 2. VII. 1929. Zbl. Neur.54, 413 (1929).

[80] Cadavid, Diego, and Alan G. Barbour. “Neuroborreliosis During Relapsing Fever: Review of the Clinical Manifestations, Pathology, and Treatment of Infections in Humans and Experimental Animals.” The Journal of Infectious Diseases, vol. 177, no. 4, 1998, pp. 1014–1032, doi:10.1086/515243.

[81] Nagel, H C. Untersuchungen uber das Verhalten des Maul und Klauenseuche-Virus im Zentralnervensystem kleiner Versuchstiere. Dtsche. Tier. Woch. 45: 624-625. (1937)

[82] Röhrer, Heinz. “Die Histopathologie Des Zentralnervensystems Bei Der Spinalen Mäuselähmung (Poliomyelitis Murium).” Virchows Archiv Für Pathologische Anatomie Und Physiologie Und Für Klinische Medizin, vol. 312, no. 1-3, 1944, pp. 740–755., doi:10.1007/bf02655974.

[83] Traub, E. Aktive Immunisierung gegen die ansteckende Schweinelähme mit Adsorbatimpstoffen. [Active Immunization against Porcine Encephalomyelitis by Adsorbate Vaccines]. Arch, wiss. prakt. Tierheuk. 77. 52-66. (1941). [Translated to English by A. Finnegan, 2019]

[84] Carbone, K M. “Borna disease virus and human disease.” Clinical microbiology reviews vol. 14,3 (2001): 513-27. doi:10.1128/CMR.14.3.513-527.2001

[85] Vilibic-Cavlek, Tatjana et al. “Lymphocytic Choriomeningitis-Emerging Trends of a Neglected Virus: A Narrative Review.” Tropical medicine and infectious disease vol. 6,2 88. 25 May. 2021, doi:10.3390/tropicalmed6020088

[86] Cain, Michaela, and Hinh Ly. “Increasing evidence of human infections by the neurotropic Borna disease virus 1 (BoDV-1).” Virulence vol. 14,1 (2023): 2218075. doi:10.1080/21505594.2023.2218075

[87] Kinnunen, Paula M et al. “Epidemiology and host spectrum of Borna disease virus infections.” The Journal of general virology vol. 94,Pt 2 (2013): 247-262. doi:10.1099/vir.0.046961-0

[88] Schäfer, W., Untersuchungen uber den Virusgehalt des Blutes und der Organe bei der Maul- und Klauenseucheinfektion von Meerschweinchen. Mhefte Vet. med. 1, 6 (1946).

[89] Kotecha, Abhay et al. “Rules of engagement between αvβ6 integrin and foot-and-mouth disease virus.” Nature communications vol. 8 15408. 23 May. 2017, doi:10.1038/ncomms15408

[90] Coburn, J et al. “Integrins αvβ3 and α5β1 Mediate Attachment of Lyme Disease Spirochetes to Human Cells.” Infection and immunity vol. 66,5 (1998): 1946-52. doi:10.1128/IAI.66.5.1946-1952.1998

[91] Sullivan, Brian M., et al. “Arenavirus Glycoproteins as Major Determinants of Pathogenicity and Host Range.” Journal of Virology, vol. 85, no. 9, 2011, pp. 4460–4469, doi:10.1128/JVI.02341-10.

[92] Pleschka, Stephan, et al. “The Borna Disease Virus Glycoprotein G Mediates Broad-Spectrum Cell Fusion and Entry via Conserved Neuroreceptors.” Trends in Microbiology, vol. 29, no. 8, 2021, pp. 712–724, doi:10.1016/j.tim.2021.01.008.

[93] Coburn, Jenifer, et al. “That’s My Story, and I’m Sticking to It—An Update on Borrelia burgdorferi Adhesins.” Frontiers in Cellular and Infection Microbiology, vol. 4, no. 41, 2014, pp. 1–17, doi:10.3389/fcimb.2014.00041.

[94] Schrauwen, Eefje J. A., and Richard A. M. Fouchier. “Zoonotic Potential of Influenza A Viruses: A Comprehensive Overview.” Frontiers in Cellular and Infection Microbiology, vol. 10, no. 9, 2018, pp. 1–18, doi:10.3389/fmicb.2018.00104.

[95] Liu, Jinyu, et al. “Pleomorphic Variants of Borreliella (syn. Borrelia) burgdorferi Express Distinct Molecular Profiles.” Microorganisms, vol. 11, no. 6, 2023, e1005759, doi:10.3389/fmicb.2023.1005759

[96] Sapi, Eva, et al. “Characterization of Borrelia-Derived Extracellular Vesicles.” Microorganisms, vol. 14, no. 3, 2026, pp. 600–615, doi:10.3390/microorganisms14030600.

[97] Long, Jason S., et al. “Host Range Barriers and Interspecies Transmission of Influenza A Viruses.” Microbiology and Molecular Biology Reviews, vol. 83, no. 2, 2019, e00054-18, doi:10.1128/MMBR.00054-18.

[98] Casselli, Tami, et al. “Coupled Induction of Prophage and Virulence Factors during Tick Feeding Facilitates Lyme Disease Spirochete Transmission.” Nature Communications, vol. 14, no. 1, 2023, pp. 1–16, doi:10.1038/s41467-023-35897-3.

[99] Jones, Robert, et al. “Characterization and Genomic Analysis of the Lyme Disease Spirochete Bacteriophage ϕBB-1.” PLOS Pathogens, vol. 20, no. 4, 2024, e1012122, doi:10.1371/journal.ppat.1012122.

[100] Trivedi, P., Wang, N. Host immune responses accelerate pathogen evolution. ISME J 8, 727–731 (2014). https://doi.org/10.1038/ismej.2013.215

[101] Casjens, Sherwood R., et al. “Inter- and Intra-Specific Pan-Genomes of Borrelia burgdorferi Sensu Lato.” BMC Genomics, vol. 14, no. 693, 2013, pp. 1–24, doi:10.1186/1471-2164-14-693.

[102] Carpi, G., Walter, K. S., Bent, S. J., Hoen, A. G., Diuk-Wasser, M., & Caccone, A. (2015). Whole genome capture of vector-borne pathogens from mixed DNA samples: a case study of Borrelia burgdorferi. BMC Genomics, 16(1). doi:10.1186/s12864-015-1634-x

[103] Trivedi, P., Wang, N. Host immune responses accelerate pathogen evolution. ISME J 8, 727–731 (2014). https://doi.org/10.1038/ismej.2013.215

[104] Doucleff, M. (2021, February 05). Extraordinary patient offers surprising clues to origins of coronavirus variants. Retrieved February 20, 2021, from https://www.npr.org/sections/goatsandsoda/2021/02/05/964447070/where-did-the-coronavirus-variants-come-from?

[105] Apoorva, and Sunit Kumar Singh. “A tale of endurance: bats, viruses and immune dynamics.” Future microbiology vol. 19,9 (2024): 841-856. doi:10.2217/fmb-2023-0233

[106] Margos, Gabriele, et al. “Borrelia bavariensis: Vector Switch, Niche Invasion, and Geographical Spread of a Tick-Borne Bacterial Parasite.” Frontiers in Ecology and Evolution, vol. 7, article 401, 2019, https://doi.org/10.3389/fevo.2019.00401

[107] Schäfer, W. (1939). Fortführung von Spirochaeta gallinarum-Stämmen von Eipassagen. [The Maintenance of Spirochaeta gallinarum by Passage in Fowl Embryos.] Vet. Bull., 11, 220.

[108] Ren, Zhongqing et al. “Organization and replicon interactions within the highly segmented genome of Borrelia burgdorferi.” PLoS genetics vol. 19,7 e1010857. 26 Jul. 2023, doi:10.1371/journal.pgen.1010857

[109] Casjens, Sherwood R et al. “Primordial origin and diversification of plasmids in Lyme disease agent bacteria.” BMC genomics vol. 19,1 218. 27 Mar. 2018, doi:10.1186/s12864-018-4597-x

[110] Stevenson, Brian. “The Lyme disease spirochete, Borrelia burgdorferi, as a model vector-borne pathogen: insights on regulation of gene and protein expression.” Current opinion in microbiology vol. 74 (2023): 102332. doi:10.1016/j.mib.2023.102332

[111] Drecktrah, Dan et al. “The Borrelia burgdorferi RelA/SpoT Homolog and Stringent Response Regulate Survival in the Tick Vector and Global Gene Expression during Starvation.” PLoS pathogens vol. 11,9 e1005160. 15 Sep. 2015, doi:10.1371/journal.ppat.1005160

[112] Grassmann, André A et al. “BosR and PlzA reciprocally regulate RpoS function to sustain Borrelia burgdorferi in ticks and mammals.” The Journal of clinical investigation vol. 133,5 e166710. 1 Mar. 2023, doi:10.1172/JCI166710

[113] Katterman, Lee. “Researchers Finding Rewarding Careers As Software Entrepreneurs.” The Scientist, vol. 10, no. 14, 7 July 1996, www.the-scientist.com/researchers-finding-rewarding-careers-as-software-entrepreneurs-1-57950.

[114] Meriläinen, Leena et al. “Morphological and biochemical features of Borrelia burgdorferi pleomorphic forms.” Microbiology (Reading, England) vol. 161,Pt 3 (2015): 516-27. doi:10.1099/mic.0.000027

[115] Bell, Graham. “Evolutionary rescue and the limits of adaptation.” Philosophical transactions of the Royal Society of London. Series B, Biological sciences vol. 368,1610 (2013): 20120080. doi:10.1098/rstb.2012.0080

[116] Carlson, Stephanie M et al. “Evolutionary rescue in a changing world.” Trends in ecology & evolution vol. 29,9 (2014): 521-30. doi:10.1016/j.tree.2014.06.005

[117] Rowe, Hannah M, and Jason W Rosch. “Polymicrobial Interactions Operative during Pathogen Transmission.” mBio vol. 12,3 e01027-21. 18 May. 2021, doi:10.1128/mBio.01027-21

[118] Beller, K. Herzwasser und sonstige tierische Rickettsiosen [Heartwater and other animal rickettsioses]. Handbuch der Viruskrankheiten (Ed. E. Gildermeister, E. Haagen, O. Waldmann). Vol. 2, Section 7, chapter 3, pp. 606-623. (1939) [Translated to English by A. Finnegan, 2021]

[119] Rodriguez-R, Luis M et al. “How Much Do rRNA Gene Surveys Underestimate Extant Bacterial Diversity?.” Applied and environmental microbiology vol. 84,6 e00014-18. 1 Mar. 2018, doi:10.1128/AEM.00014-18

[120] Margos G. et. al., Borrelia bavariensis: Vector Switch, Niche Invasion, and Geographical Spread of a Tick-Borne Bacterial Parasite. Front. Ecol. Evol. 7:401. (2019). doi: 10.3389/fevo.2019.00401

[121] Katz, Sophia et al. “Dynamics of Adaptation During Three Years of Evolution Under Long-Term Stationary Phase.” Molecular biology and evolution vol. 38,7 (2021): 2778-2790. doi:10.1093/molbev/msab067

[122] Walter, Katharine S et al. “Vectors as Epidemiological Sentinels: Patterns of Within-Tick Borrelia burgdorferi Diversity.” PLoS pathogens vol. 12,7 e1005759. 14 Jul. 2016, doi:10.1371/journal.ppat.1005759

[123] Mongodin, Emmanuel F. et al. “Inter- and intra-specific pan-genomes of Borrelia burgdorferi sensu lato: genome stability and adaptive radiation.” BMC genomics vol. 14 693. 10 Oct. 2013, doi:10.1186/1471-2164-14-693

[124] Casjens, Sherwood R et al. “Primordial origin and diversification of plasmids in Lyme disease agent bacteria.” BMC genomics vol. 19,1 218. 27 Mar. 2018, doi:10.1186/s12864-018-4597-x

[125] Stevenson, Brian. “The Lyme disease spirochete, Borrelia burgdorferi, as a model vector-borne pathogen: insights on regulation of gene and protein expression.” Current opinion in microbiology vol. 74 (2023): 102332. doi:10.1016/j.mib.2023.102332

[126] Gatzmann, Fanny et al. “NGS population genetics analyses reveal divergent evolution of a Lyme Borreliosis agent in Europe and Asia.” Ticks and tick-borne diseases vol. 6,3 (2015): 344-51. doi:10.1016/j.ttbdis.2015.02.008

[127] Andersson, Martin et al. “Multiple-strain infections of Borrelia afzelii: a role for within-host interactions in the maintenance of antigenic diversity?.” The American naturalist vol. 181,4 (2013): 545-54. doi:10.1086/669905

[128] Popov, Georgi et al. “Tick-Borne Co-Infection in Lyme Disease: Clinical Impact, Diagnostic Challenges, and Therapeutic Perspectives.” Microorganisms vol. 14,2 325. 30 Jan. 2026, doi:10.3390/microorganisms14020325

[129] Didelot, Xavier et al. “Within-host evolution of bacterial pathogens.” Nature reviews. Microbiology vol. 14,3 (2016): 150-62. doi:10.1038/nrmicro.2015.13

[130] Mongodin, Emmanuel F. et al. “Inter- and intra-specific pan-genomes of Borrelia burgdorferi sensu lato: genome stability and adaptive radiation.” BMC genomics vol. 14 693. 10 Oct. 2013, doi:10.1186/1471-2164-14-693

[131] Wróblewska-Ančevska, Anna, et al. “Organization and Replicon Interactions within the Highly Segmented Genome of Borrelia burgdorferi.” PLOS Genetics, vol. 19, no. 4, 2023, e10103936, doi:10.1371/journal.pgen.10103936.

[132] Badger, Jonathan H., et al. “Genome-Wide Signatures of Accelerated Evolution during Ecological Shifts in Bacteria.” Proceedings of the National Academy of Sciences, vol. 114, no. 38, 2017, pp. 10182–10187, doi:10.1073/pnas.1714151115

[133] Jutras, Brandon L., et al. “Borrelia Burgdorferi Peptidoglycan Is a Persistent Antigen in Patients with Lyme Arthritis.” Proceedings of the National Academy of Sciences, vol. 116, no. 27, 2019, pp. 13498–13507, doi:10.1073/pnas.1904111116.

[134] Schwan, Tom G et al. “Glycerol-3-phosphate acquisition in spirochetes: distribution and biological activity of glycerophosphodiester phosphodiesterase (GlpQ) among Borrelia species.” Journal of bacteriology vol. 185,4 (2003): 1346-56. doi:10.1128/JB.185.4.1346-1356.2003

[135] Helble, Jonathan, et al. “DnaA Modulates the Gene Expression and Morphology of the Lyme Disease Spirochete.” Journal of Bacteriology, vol. 206, no. 6, 2024, e00457-24, doi:10.1128/jb.00457-24.

[136] Liu, Jinyu, et al. “Pleomorphic Variants of Borreliella (syn. Borrelia) burgdorferi Express Distinct Molecular Profiles.” Microorganisms, vol. 11, no. 6, 2023, e1005759, doi:10.3389/fmicb.2023.1005759.

[137] Stevenson, Brian, et al. “Transcriptional Orchestration of the Segmented Genome of the Lyme Disease Agent.” Microorganisms, vol. 11, no. 10, 2023, e2439, doi:10.3390/microorganisms11102439

[138] Ouyang, Zhijian, et al. “BosR and PlzA Reciprocally Regulate RpoS Function to Sustain the Borrelia burgdorferi Enzootic Cycle.” The Journal of Clinical Investigation, vol. 133, no. 14, 2023, e166710, doi:10.1172/JCI166710

[139] “Feigned Germ War Admitted by Army: It Says It Used Nondisease-Causing Biological Substances in Eight Populated Areas between 1950 and 1966.” The New York Times, 23 Dec. 1976, p. 12, nytimes.com.

[140] Cole, Leonard A. Clouds of Secrecy: The Army’s Germ Warfare Tests over Populated Areas. Rowman & Littlefield, 1990

[141] Talagrand-Reboul, Émilie, et al. “Relapsing Fevers: Neglected Tick-Borne Diseases.” Frontiers in Cellular and Infection Microbiology, vol. 8, no. 98, 2018, pp. 1–13, doi:10.3389/fcimb.2018.00098

[142] Chaconas, George, et al. “The Dynamic and Segmented Genome of Borrelia burgdorferi: Living on the Edge.” Nature Reviews Microbiology, vol. 22, no. 4, 2024, pp. 210–225, doi:10.1038/s41579-023-00985-w

[143] Rego, Ryan O. M., et al. “The Borrelia burgdorferi Adenylate Cyclase, CyaB, Is Important for Virulence Factor Production and Mammalian Infection.” Frontiers in Cellular and Infection Microbiology, vol. 11, no. 654215, 2021, pp. 1–13, doi:10.3389/fcimb.2021.654215.

[144] Graves, Christopher J., et al. “Evidence for the Contribution of Point Mutations to vlsE Variation and for Apparent Constraints on the Net Accumulation of Sequence Changes in vlsE During Infection with Lyme Disease Spirochetes.” PLOS ONE, vol. 8, no. 12, 2013, e82423, doi:10.1371/journal.pone.0082423.

[145] Kneubehl, Lauren R., and Job E. Lopez. “Comparative Genomics Analysis of Three Conserved Plasmid Families in the Western Hemisphere Soft Tick-Borne Relapsing Fever Borreliae Provides Insight into Variation in Genome Structure and Antigenic Variation Systems.” Journal of Bacteriology, vol. 205, no. 6, 2023, e00114-23, doi:10.1128/jb.00114-23.

[146] Zhang, Jing-Ren, et al. “Antigenic Variation in Lyme Disease Borreliae by Segmental Recombination of Vmp-Like Sequence Loci.” Cell, vol. 89, no. 7, 1997, pp. 1111–1119, doi:10.1016/S0092-8674(00)80206-8.

[147] Preac-Mursic, Vera, et al. “Formation and Cultivation of Borrelia burgdorferi Spheroplast-L-Form Variants.” Infection, vol. 24, no. 3, 1996, pp. 218–226, doi:10.1007/BF01713309.

[148] Alban, P Scott et al. “Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi.” Microbiology (Reading, England) vol. 146 ( Pt 1) (2000): 119-127. doi:10.1099/00221287-146-1-119

[149] “Proceedings of the 1956 Regional meetings on Foreign Animal Diseases.” United States Department of Agriculture (USDA). Internet Archive, [Washington, U.S. Govt. Print. Off.], 1 Jan. 1970, www.archive.org/details/CAT10678014/page/102?q=Traub

[150] Jahnel F. Ueber das verhalten der geflugelspirochaten zum zentralnervensystem. Z. Hyg. Infektionskr. 112 : 613-22 (1931)

[151] Jahnel, F., Untersuchungen über die Hühnerspirochätose mit besonderer Berücksichtigung der vergleichenden Pathologie der Spirochätenerkrankungen. Wissenschaftl. Sitzg d. Dtsch. Forschungsanstalt f. Psychiatrie (Kaiser Wilhelm-Institut) München, am 2. VII. 1929. Zbl. Neur.54, 413 (1929).

[152] Nagel, H C. Untersuchungen uber das Verhalten des Maul und Klauenseuche-Virus im Zentralnervensystem kleiner Versuchstiere. Dtsche. Tier. Woch. 45: 624-625. (1937)

[153] Traub, E. Persistence of Lymphocytic Choriomeningitis Virus in Immune Animals and Its Relation To Immunity. Journal of Experimental Medicine, 63(6), 847-861. doi:10.1084/jem.63.6.847. (1936).

[154] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

[155] Traub, E., Schneider, B., Zuchtung des Virus der Maul- und Klauenseuche im bebruteten Huhnerei. [Breeding of the Virus of Foot-and-Mouth Disease Virus in Chicken Embryos]. Z Naturforsch B. May-Jun; 3 (5-6):178-87. (1948) [Translated to English by A. Finnegan (2019)]

[156] Traub, E. Aktive Immunisierung gegen die ansteckende Schweinelähme mit Adsorbatimpstoffen. [Active Immunization against Porcine Encephalomyelitis by Adsorbate Vaccines]. Arch, wiss. prakt. Tierheuk. 77. 52-66. (1941). [Translated to English by A. Finnegan, 2019]

[157] Traub, E. LCM Virus Research, Retrospect and Prospects. Lymphocytic Choriomeningitis Virus and Other Arenaviruses, 3-10. doi:10.1007/978-3-642-65681-1_1. (1973)

[158] Traub, E. & W. Schafer. Immunisierung von Mausen gegen Influenza mit Adsorbatimpstoffen von Viruskonzentraten. [Immunization of Mice Against Influenza with Concentrated Virus Adsorbate Vaccines]. Monatshefte fur Veterinmedizine. 1. 369-373 (1946). [Translated to English by A. Finnegan (2019)]

[159] RUSKA, H., & K. POPPE: Elektronenmikroskopische Untersuchungen zur Morphologie der Seiffertschen Mikroorganismen und des Erregers der Lungenseuche des Rindes. [Electron Microscopy Investigations on the morphology of Seiffert’s Microorganism and the causative agent of bovine respiratory disease]. Zeitschrift für Hygiene und Infektionskrankheiten, medizinische Mikrobiologie, Immunologie und Virologie 127 (1947), S. 201-215

[160] Traub, E., Uber die Immunitat der weißen Maus gegenüber dem EEE-Virus. VIII. Mitteilung. Zusammenfassende Diskussion. [On the immunity of the white mouse to the EEE-virus. VIII. Summarizing Discussion]. Z Immun Exp Ther. 122(3):239-58. (1961). [Translated to English by A. Finnegan (2019)]

[161] Margos G. et. al., Borrelia bavariensis: Vector Switch, Niche Invasion, and Geographical Spread of a Tick-Borne Bacterial Parasite. Front. Ecol. Evol. 7:401. (2019). doi: 10.3389/fevo.2019.00401

[162] Keller, A. et al. New insights into the Tyrolean Iceman’s origin and phenotype as inferred by whole-genome sequencing. Nat. Commun. 3:698 doi: 10.1038/ncomms1701 (2012).

[163] Hubbard, M J et al. “Distribution of Borrelia burgdorferi s.l. spirochaete DNA in British ticks (Argasidae and Ixodidae) since the 19th century, assessed by PCR.” Medical and veterinary entomology vol. 12,1 (1998): 89-97. doi:10.1046/j.1365-2915.1998.00088.x

[164] Marshall, W. F. 3rd et al. “Detection of Borrelia burgdorferi DNA in museum specimens of Peromyscus leucopus.” The Journal of infectious diseases vol. 170,4 (1994): 1027-32. doi:10.1093/infdis/170.4.1027

[165] Ibid.

[166] Persing, D., et al. Detection of Borrelia burgdorferi DNA in museum specimens of Ixodes dammini ticks. Science, 249(4975), 1420–1423. (1990). doi:10.1126/science.2402635

[167] Walter, Katherine S., et al. “Genomic Insights into the Ancient Spread of Lyme Disease across North America.” Nature Ecology & Evolution, vol. 1, no. 11, 2017, pp. 1569–1576, doi:10.1038/s41559-017-0282-8.

[168] Dumic, Igor, and Edson Severnini. “Ticking Bomb: The Impact of Climate Change on the Incidence of Lyme Disease.” Canadian Journal of Infectious Diseases and Medical Microbiology, vol. 2018, no. 5739080, 2018, pp. 1–10, doi:10.1155/2018/5739080.

[169] Humphrey, Parris T. et al. “Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis.” Evolution; international journal of organic evolution vol. 64,9 (2010): 2653-63. doi:10.1111/j.1558-5646.2010.01001.x

[170] Traub, E., Uber die Immunitat der weißen Maus gegenüber dem EEE-Virus. VIII. Mitteilung. Zusammenfassende Diskussion. [On the immunity of the white mouse to the EEE-virus. VIII. Summarizing Discussion]. Z Immun Exp Ther. 122(3):239-58. (1961). [Translated to English by A. Finnegan (2019)]

[171] Traub, E., Schneider, B., Zuchtung des Virus der Maul- und Klauenseuche im bebruteten Huhnerei. [Breeding of the Virus of Foot-and-Mouth Disease Virus in Chicken Embryos]. Z Naturforsch B. May-Jun; 3 (5-6):178-87. (1948) [Translated to English by A. Finnegan (2019)]

[172] Beller, K. Herzwasser und sonstige tierische Rickettsiosen [Heartwater and other animal rickettsioses]. Handbuch der Viruskrankheiten (Ed. E. Gildermeister, E. Haagen, O. Waldmann). Vol. 2, Section 7, chapter 3, pp. 606-623. (1939) [Translated to English by A. Finnegan, 2021]

[173] Nagel, H C. Untersuchungen uber das Verhalten des Maul und Klauenseuche-Virus im Zentralnervensystem kleiner Versuchstiere. Dtsche. Tier. Woch. 45: 624-625. (1937) [done with Traub’s assistance and further studied under Traub when he was vice president of Insel Riems]

[174] Hovind-Hougen, K. “A Morphological Characterization of Borrelia Anserina.” Microbiology (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

[175] Walker, R. L., Greene, R. T., Nicholson, W. L. & Levine, 1. F. Shared flagellar epitopes of Borrelia burgdorjeri and Borrelia anseerina. Vet Microbiol. 19, 361-371. (1989)

[176] Becker, DJ, Han, BA. The macroecology and evolution of avian competence for Borrelia burgdorferi. Global Ecol Biogeogr. 2021; 00: 1– 15. https://doi.org/10.1111/geb.13256.

[177] National Archives, Joint Intelligence Objectives Agency, J.I.O.A. Administrative Records. (1950). Memorandum on Anne Bürger, C. F. Berrens, Naval Medical Research Institute, to Chief of Naval Operations, 27 November 1950, Navy Escape Clause (RG 330). NARS.

(please note unless you open this article in Substack portions of text might get cut off in email. There are several documents shown at the end of article that will not be in the email version. Video/audio discussion of this article should be available within a few days, check back here)

Although the USDA and American government have tried to claim that Erich Traub had no connection to Plum Island, the story I have unveiled in The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare demonstrates otherwise. But there is additional information in this article that I did not include in my book with further evidence that he was in fact involved with covert testing and the setup of the Plum Island lab which at the time was known as Fort Terry. The case I make for Traub’s connection to work at Fort Terry, Plum Island is through several lines of circumstantial evidence, congressional hearings, from government officials and several biodefense sources, and secondary sources in open literature, that when put together tie together the cohesive whole.

First, we can see that in the congressional hearing from 1948 to establish a Foot-and-Mouth Disease laboratory which Plum Island was selected for, they planned to have Erich Traub there from the start, as they mention him in the hearings without directly naming him. The Congressman is asking Jacob Traum, who would later be instrumental in Plum Island research, about what happened with getting Traub to America under the Paperclip program, indicating it had an important part of the work that would be done for a FMD lab which was eventually settled on Plum Island:

Mr. Bramblett: [...] I am rather disturbed, a little bit, but I am happy that you are in it actively, [...] because I understand we lost one of the other top world experts. He came into the American occupational zone in Germany and offered to give himself up, and he did, and they immediately took him back and gave him to one of the other countries, and since then we have not heard very much about him, if anything.

Dr. Traum: Yes, he is back in the Russian zone.

Mr. Bramblett: You do not hear very much from him or what he is doing there, do you?

Dr: Traum: No. I think they are trying to put him to work there without any equipment. That is what I understand. I have not been there so what I tell you is just hearsay.1

This is exactly what happened to Erich Traub after 1945, he came and applied for work in the West to William Hagen and was turned away for his Nazi affiliations and went back to Riems where he had no equipment because the Soviets had hauled away his entire lab and put him to work with barely any equipment. Then when he “escaped” and came to America in Project Paperclip, he was initially brought to the Naval Medical Research Institute in Bethesda, MD, but he also worked with the USDA at Beltsville, MD.

Fort Terry on Plum Island was selected for special anti-animal testing activities before the USDA took over responsibilities in 1954, and although the “official” R&D work under the Army Chemical Corps did not get underway until 1952, the island was still used for temporary covert testing activities from as far back as 1944, according to a paper Medical Protection Against Brucellosis written by two military scientists with a long history in biodefense and this paper is a chapter in part of the book Biological Weapons Defense: Infectious Disease and Counterbioterrorism a textbook for biodefense specialists and put together by people with a background in biodefense, they show that it was used for testing since 1944:

In November 1942, Secretary of War Stimson requested the Chemical Warfare Services (CWS) to prepare to assume responsibility for biowarfare research and development under the supervision of the War Research Service. Subsequently, the Army chose Camp Detrick in Frederick, MD, as the site for the biowarfare research program, and construction began in April 1943. The emphasis of the program was protection of soldiers. To achieve this goal, CWS created the Special Projects Division (SPD). The SPD built and operated numerous of facilities, including Camp Detrick in April 1943 with the parent research and pilot plant; Field Testing Facility in Horn Island Mississippi in June 1943; Vigo Ordinance Plant in Terre Haute, IN in May 1944; Granite Peak Test Site at Dugway Proving Grounds for field testing in June 1944; and Fort Terry in Plum Island, NY for Veterinary Testing in 1944. Work with brucellosis performed at Camp Detrick and Dugway Proving Ground during the war was focused on aerosol dispersion patterns, infective dosages, and development of vaccine products in an attempt to develop countermeasures and offensive weapons.2

The building that was known as Building 257 (which was laboratory 257 when the Army Chemical Corps was using it prior to transferring it over to the USDA in 1954) was already built in 1911, so it was not merely built in 1944 to be used later, it was approved for veterinary testing of biological agents that year. Further clues about Fort Terry activities in antianimal research & development (R&D) biowarfare research were disclosed in Deadly Cultures: Biological Weapons Since 1945:

The US antianimal [Biological Warfare (BW)] program featured at least one dedicated facility and the development of four agents and a number of delivery systems. Antianimal BW were viewed as strategic instruments to be used to reduce enemy food supplies or to cause economic damage […].

The US was bound by federal statute banning research with certain highly infectious animal diseases within the continental United States. This limitation was initially overcome by carrying out work offshore at Plum Island, New York, and later by coordinating antianimal activities with allies.

Antianimal R&D was initiated as a result of a study conducted by the Operations Research Office into the offensive potential of such agents. The report concluded that because of the importance of livestock in the economy of the USSR and the feasibility of developing the necessary capabilities there was a need to develop antianimal BW. This decision was followed by “a firm requirement for offensive munitions and agents for use against horses, cattle and swine” from the US Air Force. The US Army Chemical Corps responded by assessing a number of potential sites to conduct the necessary R&D and in 1952 selected Fort Terry on Plum Island, New York. Existing plans by the US Department of Agriculture (USDA) to build an animal disease research facility on the island offered the advantage of common utilities, including a steam plant, decontamination plant, and water system.

Plum Island lies in Long Island Sound, Suffield County, New York, and covers about 840 acres. It is about 2.5 miles long, tapering from a width of one mile at one end to around 800 meters at the other. It possesses a natural harbor. The Chemical Corps facility covered about 3 acres and included laboratories, animal houses, administration buildings, communication buildings, a hospital and fire station, a motor pool, a dock, ware housing, staff quarters, a commissary, cafeteria, and guardhouses.

Fort Terry was activated on 15 April 1952 as a permanent installation under the control of the Chemical Corps but under the custody of the First Army. Its originally scheduled opening, on 1 March 1952, was delayed by protests from local residents against the USDA’s plans. At its inception, it was planned that 9 military and 10 civilian personnel would staff Fort Terry. By the time it was deactivated and transferred to the USDA in 1954, it had at least 9 military and 8 civilian personnel. Another 162 people were directly contracted to service the facility. Records and files from Fort Terry were transferred to Camp (later Fort) Detrick, which retained responsibility for antianimal BW development, and many were later destroyed.

The mission of Fort Terry was “to establish and pursue a program of research and development of certain anti-animal (BW) agents.” Foot and mouth disease (FMD) virus was the first candidate agent for development. Fort Terry was also charged with screening other exotic animal diseases for potential as BW agents. It appears that development of the causative organism of rinderpest (a disease of cattle) had already been achieved in Project 1001, which took place outside the US. During its operation, personnel from Fort Terry were involved in collaborative exchanges with other facilities, including the FMD laboratory at Pirbright in the UK. The inventory taken at Fort Terry before its deactivation reveals the presence of 15 agents and antisera for many of them (table 11.1). Antianimal activities, however, were not limited to Plum Island. A 1950 overview of the operational divisions present at Fort Detrick indicated the presence of V and C Sections, representing veterinary and crop capabilities.

Despite the early interest in this form of warfare, by 1952 antianimal BW had been dismissed as “relatively insignificant,” and military support for R&D was withdrawn in September 1953. This move followed a report by the Joint Staff Planners in August asserting that the US military had “no capability in anti-animal BW,” a claim that contradicted documentation from Fort Terry. There was a resurgence during the years that followed, however; a 1957 Air Force historical study of US BW activities indicated that two weapon systems had been successfully tested for use with antianimal agents .

Contemporary studies of this program provide additional details of these antianimal activities. Agents were arranged into three schedules that presumably related to desirability and utility: schedule 1 contained foot and mouth disease and rinderpest; schedule 2 included classical swine fever (hog cholera), fowl plague, and Newcastle disease (of fowl); and schedule 3 consisted solely of wart hog disease (African swine fever). In addition, the antianimal utility of anthrax and Venezuelan equine encephalitis were noted.

Four weapon systems suitable for use with these agents were developed:

• Spray tanks, developed by a commercial corporation for use by the Navy with hog cholera and Newcastle disease

• Balloon bombs, codenamed E77, for use with a variety of agents and considered a strategic weapon

• Feather bombs, codenamed E73, which were developed from a leaflet dispersal device and contained four packets of inoculated feathers

• Particulate bombs, which were still under development in 1950

As well as these four military delivery devices, antianimal agents were considered for sabotage operations. The 1950 Creasy report asserted that covert contamination of animal food should initiate an animal disease outbreak and that contamination with certain agents would also prevent the reestablishment of animals in certain areas. Such capabilities, the report declared, were easily attainable. It has proved difficult to trace the history of antianimal biological sabotage because, although there are references to sabotage capabilities, there are few details about what these were or how, why, or when they were developed, and if they were used. […] 3

We know from books like The United States and Biological Warfare: Secrets from the Early Cold War and Korea that they were also loading up bomblets with insects and ticks used in the Korean War,4 which would have been right in line with what I have proposed about Traub’s line of work while in America on biological warfare, and we know from the FBI files that Nazi scientist Dr. Theodor Benzinger worked with Traub conducting tests with him for Detrick, and Benzinger was a medical researcher centered around aviation and aerodynamics, so there was collaboration with him most likely on how to produce these various types of bomb devices for work under Detrick’s biowarfare program.

There was also a table included in Deadly Cultures listing biological agents that were housed at Fort Terry prior to the transfer to the USDA in 1954:

Most of these agents Erich Traub specialized in, such as Foot-and-Mouth Disease, Vesicular Stomatitis Virus, Rinderpest Virus, Teschen Disease Virus, Fowl Plague Virus, Newcastle Disease Virus, and most notably, “N” Virus which was discovered by Erich Traub’s protégé Zvonimir Dinter back at Insel Riems in the late 1940s,5 and Traub would have been the one to give the Americans their only strain of it. Traub had been working on Vesicular Stomatitis with USDA official L. O. Mott in 1950 at the Beltsville station of the USDA in Maryland.6 Mott was heavily involved in the USDA’s tick-borne disease programs and attended several USDA conferences on Anaplasmosis throughout the 1950s,78 as well as transmission studies and antigen production/compliment fixation tests.910 No other Nazi scientist in the Paperclip program had this type of expertise on any of these viruses, especially on the level of Erich Traub. Erich Traub was internationally known and sought after by many nations, and was also a mentor to the researcher who discovered Virus N.

Even though the USDA did not take over responsibility for the island’s activities until 1954, and even though the Army Chemical Corps turned Fort Terry into a permanent research facility in 1952, they certainly would have been using the island for temporary clandestine research of a highly classified nature since 1944, especially if it was by special intelligence divisions, and as the record stands, many records that were available on Fort Terry Plum Island research “were later destroyed.” This is important because it shows there were things to cover up to avoid transparency, in which they began destroying evidence and records of it. It is also telling that around this time they claimed that there was no capability in anti-animal bioweapons research despite records from Fort Terry indicating otherwise. This shows dishonesty and an attempt to conceal aspects of the research done there.

Regarding potential CIA/Intelligence involvement at Plum Island we might look to people like Frank Olsen, the Camp Detrick biochemist thought to be killed by the CIA after unwittingly drugging him with LSD, and was thought to have been recruited by the CIA. We find some very interesting clues about Plum Island beyond what is in public records and more testimony from Detrick personnel placing Traub on Plum Island in 1951. In H. P. Albarelli’s work on Olsen, published in his book A Terrible Mistake: The Murder of Frank Olson, and the CIA’s Secret Cold War Experiments, it states in that book that Frank Olsen was working at Plum Island in a limited capacity with Erich Traub:

On at least five occasions, spread out over 1951, 1952, and early 1953, Frank Olson, journeyed by military aircraft to Fort Terry on Plum Island, off Long Island, New York. The 840 acre island, purchased by the U. S. War Department in 1901, is only about 135 miles from New York City. In 1951, the Army Chemical Corps selected Plum Island as a non-animal research and development site, so as to sidestep federal laws, banning experiments involving certain highly infectious animal diseases within the continental United States. After spending millions on the Plum Island facility and arousing stiff opposition from nearby mainland residents, the United States Department of Agriculture took the island over from the Army Chemical Corps in 1954.11

Its unclear why he said “non-animal” research and development site to test animal diseases, but that could have been a typo on his part, unless they were working on these animal diseases for human use like I have maintained that Traub was adapting animal diseases to humans and the insect simulant program could very well have been touted as a covert vaccine program. At any rate, it further states:

Also, assisting Olson and his colleagues, and their Plum Island activities were doctors, William Arthur Hagen, and Erich Traub. Dr. Hagen, A key advocate for the creation of the Plum Island Experimental Station, was dean of the Cornell University veterinary school in Ithaca, New York, and a renowned authority on Bacillus anthracis (anthrax). […]12

Olsen was involved in work at Plum Island setting up the laboratories with Traub and others from U. S. Biodefense and were there since 1951, the same year a former Plum Island source in Carroll’s book Lab 257 said Traub was there with other scientists inoculating ticks and releasing them on the island for simulant tests. Albarelli’s sources for the information about Olsen’s work at Plum Island seem to have come from one or all three Detrick colleagues, such as Don Falconer, Dr. Gerald Yonetz, and Dr. Henry Eigelsbach. Unfortunately, Albarelli was not as exact in sourcing as I like to be. However, it further states that the biowarfare research done there was much more extensive than the public knew. Olsen was also part of the Special Projects Division (SPD) of the Chemical Warfare Service (CWS), which was the same division cited earlier that decided to use Fort Terry for veterinary testing in 1944. He was said to have been there since 1951 so it was clearly being used before 1952 as a temporary facility for covert testing.

Interestingly, it also states that Olsen was involved in the open-air testing of the simulant bacteria Serratia marcescens in California.13 Traub’s role as “Supervisory bacteriologist” to include the overseeing and facilitation of the simulant testing and working with people like Frank Olsen to facilitate and assist in it is exactly what I have maintained Traub was doing in The Sleeper Agent, and as Carroll wrote in Lab 257 he was at Plum Island in 1951 to conduct insect simulant tests:

Traub might have monitored the tests. A source who worked on Plum Island in the 1950s recalls that animal handlers and a scientist released ticks outdoors on the island. “They called him the Nazi scientist, when they came in, in 1951 — they were inoculating these ticks,” and a picture he once saw “shows the animal handler pointing to the area on Plum where they released the ticks.” Dr. Traub’s World War II handiwork consisted of aerial virus sprays developed on Insel Riems and tested over occupied Russia, and of field work for Heinrich Himmler in Turkey. Indeed, his colleagues conducted bug trials by dropping live beetles from planes. An outdoor tick trial would have been de rigueur for Erich Traub.14

Even though the term “supervisory bacteriologist” is not under normal circumstances a title designated for simulant tests in average science positions, it is certainly activity that could be included in that roll if it was in a military or biodefense capacity.15 These type of vague titles would be commonly used to keep that work undisclosed in the job title. As for the open-air simulant tests with Serratia marcescens, it was suggested to us by Kurt Blöme in his interview with American Intelligence to enter the Paperclip program,16 and Traub had weaponized the simulant bacteria Serratia marcescens while back in Germany in 1940 with bovine papular stomatitis virus.17 Its possible he could have been telling the U.S. it was a vaccine against smallpox, and it is possible he could have been touting the ticks in a similar way, as even recently they are talking about using insects to spread vaccines,18 and it is likely because they had already been attempting it.

Traub had applied for employment at Plum Island in a 1958 form,19 that I initially thought was a security investigation for him to visit the United States to attend a virology institute and listed employment for Plum Island. It was a reasonable mistake because on the form all I could read was “Security Investigation” and the part “…for Sensitive Position” was nearly illegible and I didn’t catch it until recently. He was attending a virology conference that year in New York, and he was under surveillance for the remainder of his life, so I mistakenly thought this form was to give him permission to visit the United States when it was actually one of his applications to lead Plum Island, but it does not change the story that he was very involved in Plum Island anti-animal testing activities from when he arrived here in Paperclip, even though he was only traveling there on certain occasions, as they were limited tests. The fact that he was being asked to lead Plum Island by multiple people within U. S. biodefense like Richard E. Shope,20 suggest that he was already instrumental for the supervision of any of the work done there prior to 1954 in a more classified setting.

Its unclear why this application was made to Plum Island at this point, because of all that had already gone down during his Paperclip tenure, but he was not given the role, even though it seems that he wanted it badly, because he voiced these desires in files available in his embezzlement investigation in 1959, one year after the application was made.21 22 Although I originally thought he ultimately declined to lead it in 1958, he was more likely turned down. Perhaps it was a last ditch effort to get himself out of the hot water he was already in at the Tübingen animal disease institute he was leading, since he was under investigation for embezzlement and looking at jail time.

Next, notice that the quote I provided from Deadly Cultures shows that Fort Terry was involved with joint research with British scientists in joint research. Although it does not say that the British were at Plum Island, they were involved in joint programs that included Fort Terry and could very well have been there during these earlier covert testing activities, and it lends more weight to the claim by John Loftus and his source in biodefense, who I did meet personally, who maintained that British Intelligence were involved in some of the joint-testing activities at Plum Island from early on. It was one of the ways they circumvented restrictions on biological testing in America forming this tripartite agreement joint research with Canada and Britain.

And although I have mentioned Donald Maclean possibly directing some of these tests, I did not mean he was directly involved in carrying them out or even witnessing them personally, I meant he was directing intelligence divisions below him to facilitate the testing at Plum Island, I never said he was directly doing any of the experiments himself or even at Plum Island in person, I meant he was merely coordinating with Intelligence agencies and military that they should be done by the right outfits and scientists in biodefense.

So, we can conclude this article by saying that at least 3 scientists who were Camp Detrick personnel,23 as well as my biodefense source who held a Q clearance, who is also the source that John Loftus was drawing from as he states in the introduction to my book, along with the anonymous source from Lab 257 who worked at Plum Island, say that Plum Island was operational before 1952 and at least one of these sources say coordinating the work with Erich Traub. The biodefense source I met was also the source of John Loftus’s original claim in The Belarus Secret, not the CIA personnel who was clearing his book.

But again, Traub’s work at Plum Island during the Paperclip Program, does not mean he spent a whole lot of time there. I probably should have clarified this in my book that it was not a place they would remain for long periods of time and Traub would not be working on the island the entire time he was in America. He would have been there for specific tests and it would be a limited stay. But these limited trips to Plum Island certainly would have spanned his entire stay in the Paperclip program.

They were planning to eventually have him there permanently if he had not been sent back to Germany, but he would have been instrumental in assisting Frank Olsen in 1951 to advise on its setup because he was having them model it after the setup on Insel Riems, which is like the German version of Plum Island. Erich Traub was very important for this reason alone. Not only was he an expert on preparations for biological warfare like it says in his intelligence file, but he would have had additional expertise on the facilities, setup, and equipment needed to run it.

Because Plum Island was so desolate, took a considerable time to get to, security so extreme, it would not have been a place that Traub or anyone else would want to be staying for long periods of time, there was nothing to do there beyond the experiments and no reason to stay there for extended periods of time, so they would have only taken trips there on certain occasions to conduct very important covert research in the years before it was setup as a permanent facility in 1952 doing official research. Olsen’s colleague mentioned in Albarelli’s book how stressful being there was and how it really put him to the test being there to setup the ventilation system:

Olsen’s task on Plum Island was to “review the installation of ventilation system, security, and safety.” Overall security at Plum Island was intended to be even tighter than at camp Detrick. Indeed, Olsens colleague, Dan falconer said in 1999:

Frank remarked a couple of times that he was really put to the test working at Fort Terry. Just getting to the island was a difficult task and, once there, security was relentless. There were guards everywhere constantly patrolling the shores and perimeter. Frank, I think, like everyone who worked there, hated the weather and the boredom. He only went there when he had to.24

In conclusion, I think there is considerable corroborating evidence that shows not only was Plum Island being used before 1952 as far back as 1944, it was definitely being used by 1951 when Traub was there working with scientists like Frank Olsen and this lends considerable weight to the theme that even though his cited task on Plum Island was to set up the facility, he was also there for insect simulant tests that Traub was assisting and supervising, just like Frank Olsen was involved in the open-air simulant tests in California that I have maintained Traub was also a part of since the Serratia marcescens testing was suggested to us by the Germans and he had experience with this pathogen, and had a diverse background working with diverse pathogens from his time in Germany and at the Rockefeller Institute.

They were using the island for covert testing and of a highly classified nature, hence the high security, and thus the reason why we generally can’t find it in the public record. That’s the nature of this kind of work and why it is so hard for researchers to paste together a definitive history because it is all covert, classified programs that will probably never be released to the public if any even remain in existence, as much of it has been shredded, and probably for a reason. But not every detail was able to be shredded when its coming directly from personnel and this is why it is important to listen to whistleblowers from within the government and laboratory personnel because they still have facts that the powers that be could not make disappear, and it is important that we listen to them when they speak up, not simply write them off as unreliable because their testimony is unsettling, because the government itself is not going to tell us the truth on the matter that we may have a very real need to know.

Further Documents:

Traub applied for American work in 1945 and met with William A. Hagen for potential work in the Paperclip program, showing the congressional hearing was about Erich Traub. This is from FBI file on Traub’s Loyalties:

Also from FBI file, this shows that he was conducting experiments with high-altitude medical specialist Theodor Benzinger, who said his lab was hauled off by the Russians (thus, why they were trying to put him back to work there without any equipment):

From CIA file, showing they put Riems back to work after dismantling the laboratory:

Declassified files from National Archives on his Joint Intelligence Objectives Agency file, prove that Erich Traub’s work in the Paperclip program was directly related to biological warfare, and shows that he was one of a kind, a talent and authority on biowarfare that no other personnel available in the United States could fill :

National Archives. Joint-Intelligence Objectives Agency file on Erich Traub (RG 330). NARS. Joint Intelligence Objectives Agency (JIOA), JIOA Administrative Records. (1949-54).

His fundamental research was in virology but he was given the title of supervisory bacteriologist, which would be fitting for his overseeing bacterial simulant tests, even if not under normal circumstances a title that involves simulant testing, but at this time and in a military position this would be common to use a vague title like supervisory bacteriologist for supervising bacterial simulant testing:

National Archives. Joint-Intelligence Objectives Agency file on Erich Traub (RG 330). NARS. Joint Intelligence Objectives Agency (JIOA), JIOA Administrative Records. (1949-54).

Here is the Navy’s request for employment of Anne-Lise Bürger specifically for the purpose of assisting Dr. Traub for the purpose of biological warfare research & development, this is the entirety of the following file:

National Archives, Joint Intelligence Objectives Agency, J.I.O.A. Administrative Records. (1950). Memorandum on Anne Bürger, C. F. Berrens, Naval Medical Research Institute, to Chief of Naval Operations, 27 November 1950, Navy Escape Clause (RG 330). NARS.

Front page of paper showing Traub’s collaboration with L. O. Mott, that although it wasn’t published until 1958, the work was done starting in 1950 at Beltsville station of the USDA

Here at the bottom of the above paper it says the work was from 1950:

Pictures of tick and insect bombs used by the United States in the Korean War from book - Endicott, Stephen, and Edward Hagerman. The United States and Biological Warfare: Secrets from the Early Cold War and Korea. Indiana University Press, 1998 :

From The United States and Biological Warfare: Secrets from the Early Cold War and Korea : by Stephen Endicott and Edward Hagerman

Dr. Blome’s Interview with American Intelligence about simulant tests with Serratia marcescens:

Endnotes

By “duplicating” I mean the same practice - repeated rearing and inoculating of tick vectors and packing them with a myriad of viral, mycoplsmal, bacterial, and rickettsial pathogens and releasing them into the environment - something that never would have happened under natural conditions and thus cannot be seen through the eyes of natural evolution by any stretch of the imagination. This brings highly unusual man-made conditions that span globally taking each their own evolutionary path in their respective ecosystem, and no studies in phylogenic evolutionary relationships have ever considered and incorporated such elements into the arrangement of bacterial phylogenies.

In saying that Lyme disease was closest to the avian relapsing fever Borrelia anserina, I need to clarify that I meant the entire Lyme Borreliosis clade,2 but apparently I was not clear enough in making that point so there has been some confusion. Borrelia burgdorferi is obviously closer to some of its sibling species in the Lyme Borreliosis clade, like Borrelia afzelii, Borrelia garinii, among others others, which Borrelia anserina served as an outgroup. I am saying the entire Lyme clade came from Borrelia anserina and it was engineered in just a few years through highly unique and sophisticated conditions that bypass natural evolution and create conditions that have never been openly studied in the context of a man-made phenomenon. This is especially unique when the ticks carrying such a sophisticated mix of new infections are then introduced into many new climates across the globe by man - determined to advance their biological warfare capabilities and biodefense programs on multiple parts of the globe simultaneously.

It does not mean Traub engineered each species of the clade himself, it could have been just one or two species that when shared with other superpowers or introduced into different climates or ecosystems - rapidly evolved due to the unusual nature of the multiple pathogens it was growing with in new vectors that are immune tolerant, along with co-infecting mycoplasma and bacteriophage varieties. It is known that viruses rapidly mutate in the immunosuppressed and this could also create highly unusual conditions for unprecedented rapid evolution of bacterial pathogens into what appear to be new species and sub-species evolving from just one species - Borrelia anserina - in a short amount of time, and yes, a span of just several years, not hundreds, thousands, or millions of years. We are talking many jumps in a short timeframe - new tropisms, hosts, vectors, and resistance genes to antibiotics. These are all traits that Traub specialized in and added to its engineered evolution. Taken together, this could completely remodel a species into entirely new clades separated by what appear to be long-term evolutionary distances when in fact it was very short-term changes in sophisticated growing conditions enabling diverse mutations and rapid evolution that when released in diverse ecosystems across the globe, would further evolve in highly unique and unprecedented ways.

However, it brings up an important point; we only use bacterial phylogeny as a rough guide in reconstructing the split between the Lyme Borreliosis clade and Borrelia anserina in the context I put forward in The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. But this rule of thumb is also true for all scientists to go by. The phylogenic tree should never be treated as a fully conclusive end all be all. It is not an absolute, and in fact there are many elements that can skew the phylogenic data. In this article, I will explain in greater depth why that is the case, and why such unusual man-made adaptations coupled with sophisticated growing environments could have allowed for rapid transformation and evolution of the Borrelia anserina pathogen to give the appearance of multiple species across the globe whose genetic profiles seem much further in distance between the species than they actually were.3

My book’s evidence does not document every step and provide hard evidence on each point along the way showing how this was done. My job is to look at the big picture of a highly secretive and sophisticated form of warfare with microbiology and reverse engineer the story based on available evidence and testimony, just as a scientist would do in recreating long-term evolutionary history. I rely on the extensive, overlapping circumstantial evidence in toto to make my case, thus, in a way that explains the entirety of the picture without contradiction, and by doing it this way - it leaves a far more solid tapestry based on available evidence than by relying on bacterial phylogenies alone which are also built on theories and inferences that are anything but absolute and assume no man-made conditions or anomalies were involved other than steady long-term evolution in a natural habitat over millions of years. We know this to be wrong when looking back at the history of the biological warfare race.

The entire study and assembly of bacterial phylogenic trees has been done in times where man was heavily influencing the environment and studying microorganisms in controlled laboratory conditions, so to look at phylogeny as a concrete marker of natural evolution would be almost ridiculous when you take into consideration how much influence we have had on environments and microbes since modern science began. They’ve never had control samples to compare to when microorganisms were actually thriving in a natural habitat free of man-made influence and controlled laboratory conditions.

Many scientists have even argued that bacterial phylogeny as an evolutionary tree is insufficient and must be uprooted as a model because bacterial lifeforms are chimeric, they are subject to Horizontal Gene Transfer (HGT) inheriting DNA and genetic material from unrelated bacteria, and even the so-called stable 16S rRNA operon used as the gold standard for reconstructing bacterial phylogenies is far more malleable than initially thought. The 16S rRNA operon is in fact amenable to Horizontal Gene Transfer,4 which means you can’t depend on phylogenic trees alone and shows its limitations to be significant, as the 16S rRNA gene is much more prone to rapid evolutionary changes the prokaryotes are than the higher forms of life such as mammals that undergo sexual reproduction and vertical gene transfer. Therefore, making the analogy between the distance of man and chimps compared to bacteria simply does not work here.

Especially noteworthy is that giving bacteria antibiotic resistance genes can mutate the 16S rRNA genes considerably and there is some evidence that suggests Traub was already adept at working with such environments and we know this to be an important target for biological warfare research and development. Another limitation in solely relying on the phylogeny is that there was no sequencing of the earlier strains used, such as the Borrelia anserina that Werner Schäfer and Erich Traub began maintaining in 1939 from Franz Jahnel.5

Furthermore, there are elements of this story that no one has ever studied – mainly in the highly sophisticated conditions created by Erich Traub and his German colleagues during WWII, when he began adapting multiple overlapping infections from different sources into the same tick vector like a Russian-doll cocktail, with the addition of bacteriophage varieties (including lyophilized or dry-frozen bacteriophages),67 viruses,8 and mycoplasma,9 all of which Insel Riems was working with during Traub’s tenure as Vice President - overseeing the entire phase of Insel Riems research in the WWII years and well into the beginnings of the Cold War under Soviet occupation. The addition of viruses, phages, and mycoplasma would act as gene shuttles between the different co-infecting agents, allowing for rapid evolution and gene swapping between numerous foreign pathogens that had not been exposed to each other previously. Such controlled environments could greatly accelerate mutation rates, adapt pathogens to many new hosts, change its tropisms, and take on a myriad of new characteristics - making short-term changes appear to be long-term evolutionary distance.

To add another layer of complexity, once these extremely unique and unusual biological specimens were introduced into wild habitats of ecosystems in vastly different parts of the globe by nations duplicating or conducting further biowarfare research and testing activities, it further complicates the theory of natural evolution with yet even more highly divergent and unique conditions from the native viruses and microbes in each specific ecosystem where these vectors are released. This could diversify further what seem like millions of years of evolution when in fact were just a few years of highly exceptional conditions duplicated across varying climatic conditions within a few years in their respective biological warfare programs.

Absolutely none of this type of unusual man-made biodefense activity was factored into the equation by academic researchers reconstructing bacterial phylogenic trees, making an already limited theoretical framework vulnerable to be skewed a thousand ways to Sunday. We like to think that we can just go to GenBank and see definitive ancestral relationships, timelines, and evolutionary distances - when in fact this is not necessarily the case.

We need to also consider all the additional evidence - as well as the underlying motivations showing the desire and intent to modify specific agents like Borrelia anserina were present. A growing demand to completely remodel the pathogen, change its pathogenic properties, tropisms, adapt it to new hosts, add antibacterial resistance genes, all as far back as in the days of WWII. Borrelia anserina is a case in point, because there was a growing demand to do this to Borrelia anserina in pre-WWII Germany at the time.

As is common in top secret research and development, advances in science were often known many decades before their public disclosures. I believe Insel Riems and the Germans were already up to speed on current modern-day bioengineering back in the days of World War II, as Insel Riems was working with several bacteriophage varieties and Mycoplasma. Both would act to shuttle genes between the different cocktail of pathogens and accelerate rapid evolution. I believe adding bacterial resistance was already a known skill by Erich Traub. Perhaps this is why his son Walter then went on to spend his entire life studying antibiotic resistence in simulant strains of bacteria like Serratia marcescens.

Erich Traub had also known that he could use viruses to adapt microorganisms to new species of animals through the formation of heterokaryons. He likely taught this technique to Iranian scientist G. K. Kanhai while in Iran in the late 1960s - teaching him how to change the properties of FMD virus to take on a whole array of new properties, adapt other pathogens to new species and beyond. As Traub said in his collaborative work with Kanhai, just some of the factors he was able to change with ease were:

a) natural retrogression and termination of epizootics;

b) increase in potency of the causative agent;

c) virus adaptation to certain species of animals and escalation or decrease of infectivity and pathogenicity for other species;

d) different affinity of virus strains for certain cells (cardiac FMD);

e) differences in susceptibility among individual animals of the same species;

f) reduced susceptibility in undernourished individuals;

g) different behavior of different virus types;

h) persistent infection;

i) serological variation.10

Some years later, Kanhai then went on to publish about the use of Sendai virus to adapt the tick-borne disease Theileria parva to a new host via cell-fusion, or the creation of heterokaryons.11

Remodeling Borrelia anserina: A Growing Demand in Nazi Germany

When Erich Traub had Werner Schäfer acquire and maintain Borrelia anserina from Franz Jahnel in serial egg passages for his institute starting in 1939, several attempts had already been made previously trying to adapt Borrelia anserina to a variety of new hosts like mice and other animals, change its tropisms to be more neurotropic in order to serve as a comparable animal model for the study of syphilis. This was noted by Franz Jahnel in a section of a 1936 book titled 25 Years of the Kaiser Wilhelm Society for the Advancement of the Sciences (25 Jahre Kaiser Wilhelm-Gesellschaft ƶur Förderung der Wissenschaften), in a section titled Institute for Spirochetal Research (Institüt für Spirochätenforschung). He cites numerous attempts to adapt the avian spirochete to mice, lizards, turtles, frogs, fish, and pigeons by other researchers.12 This shows the desire to adapt it to new hosts and remodel it altogether was already in growing demand before WWII.

Erich Traub had a specialty in the art of adaptation, and he was involved in having an Insel Riems associate Hans Cristoph-Nagel adapt FMD Virus to mice, completely changing its qualities to become highly neurotropic,13 turning it into a central nervous system disease after the 140^th+ passage when it previously was a disease that caused blisters on the mouth and hooves of cattle.14 This adaptation occurred when Traub visited the Insel Riems facility on a return visit from the Rockefeller Institute in the years 1936-37 and brought mice from the Rockefeller Institute to Nagel, likely infected with the LCM virus and served as a helper virus to assist the change.15 Traub then adapted FMD Virus to chicken eggs when no one else had been successful in their attempts. He did this by mixing 12 different variants of FMD Virus in one egg and alternating passages between the egg and guinea pig to get the virus slowly used to the egg until it was fully adapted to the egg.16

In 1936, a German researcher Margeret Zuelzer had found a new vector for Borrelia anserina in the Culex mosquito,17 so there was an obvious demand not only to change its host and tropisms to be more like syphilis, but to also find new vectors to transmit the spirochete. Taken altogether, this would require a total makeover of the pathogen which could have easily mutated the 16S rRNA operon which the phylogenic trees are assembled based on under the false assumption that they are immune to horizontal gene transfer.

The next important part of this timeline is when Erich Traub was gaining unique tick-borne disease expertise as assistant professor to Dr. Karl Beller in 1939. In a chapter Heartwater and other animal rickettsioses (Herzwasser und sonstige tierische Rickettsiosen) from the Handbook for Viral Disease (Handbüch der Viruskrankheiten) published in 1939 by Karl Beller, he studied complex systems of multiple infections (Babesia, Bartonella, Ehrlichia, Rickettsisa, and Leishmania) all rolled into one host and had the foreknowledge that it was possible to transmit relapsing fever spirochetes through hard-bodied ticks like the brown dog tick.18 Since Erich Traub was working with him at the time as assistant professor he would have gained expertise from Beller’s studies of tick-borne disease. We later find all the same co-infections infecting hard-bodied Ixodes ticks in Europe and North America when he was brought to the United States in Project Paperclip, and not long after that the Lyme explosion began. He merely swapped Leishmania with a completely remodeled Borrelia anserina. This interesting chapter demonstrated that when such a complex of multiple overlapping co-infections were produced, it caused immune tolerance, which had sometimes been called prämmunity.

This would most likely be true for the tick as well, where a tick carrying multiple overlapping pathogens from foreign sources is immunosuppressed by the cocktail of infections. It is known that viral mutations happen rapidly in immunosuppressed hosts,19 and this would create a synergistic effect for the spirochetes and other co-infecting pathogens. No one has ever studied how this affects the evolution of specific pathogens in relation to assembling bacterial phylogenic trees. Therefore, the bacterial phylogeny of the Lyme Borreliosis clade of Borrelia cannot be seen through the lens of natural evolution and its rapid evolution is vastly different than than that seen in any kind of basic serial passage of a single species of microorganism grown on their own in a single type of animal.

Insel Riems was a state-of-the-art facility at the time and had been doing work on mycoplasma and bacteriophages, and they had the capability to completely remodel Borrelia anserina as was in growing demand at the time. It was known that Germany was conducting all the same simulant tests in WWII that Traub would later supervise in the United States, as Kurt Blöme’s file shows.20 The Germans had actually started this kind of testing in the subways of London and Paris in the 1930s.21 It is also very likely that the Japanese duplicated these tests as they were sharing at least some of the important chemical and biological warfare intelligence,22 and this is why the Lyme clade includes some species from Japan. Traub and Karl Beller had been citing Japanese research using different insects to transmit Equine Infectious Anemia Virus in 1942.23

The Soviet Union captured Insel Riems in 1945 and hauled off the majority of their lab equipment and research records that was done up to 1945,24 so the Soviet Union would have certainly been further developing and testing this unusual cocktail of infectious disease in vectors in the Soviet Union,25 further diversifying the lineage of remodeled Borrelia anserina – the Lyme Borreliosis clade coming from Borrelia anserina as an outgroup.

Project Paperclip and Plum Island Work

When Erich Traub was brought to America in Project Paperclip he was brought here and worked with the USDA at Plum Island from the beginning,26 and even before he was brought to the USA the congressional record shows that they were planning on having him working at Plum Island under the law that established the laboratory for work on FMD and foreign animal diseases when they mentioned him in the hearing, not by name, but by other recognizable elements to reveal his identification, such as calling him the world’s top specialist of FMD, but they said he had applied for work in the West but was rejected for his Nazi affiliations and returned to the Russian zone, which is exactly what happened to Traub before Soviet moles in MI6 facilitated his phony “escape” in 1948.27

Erich Traub filled out an application to lead Plum Island in 1958, initially I thought this was a security investigation to visit the United States as he was attending a virology conference that year, as the second half of the title of the form “for Sensitive Position” was nearly illegible. He cited the public law 496 80th congress - establishing an FMD lab - as the reason for appointment and that hearing in 1948 spoke about putting Traub there directly even if not by name. Plum Island was used for veterinary testing since at least 1944,28 so it would have been a desirable place to conduct anti-animal tests and he would have been involved in any work there from his earlier days in Paperclip.29

In his Joint Intelligence Objectives Agency (JIOA) file, Traub attended a conference in Washington D. C. in 1950 during his Paperclip tenure and listed B. T. Simms of the USDA as a point of contact if anyone needed to get in touch with him. Simms was a USDA official who was involved in some of the research at Plum Island.

Furthermore, a paper Traub co-authored with Lawrence O. Mott from the USDA on Vesicular Stomatitis, published in 1958, shows that Traub was working with the USDA at the Beltsville station of the Agricultural Research Service (ARS) which at that time would have been the Bureau of Animal Industry (BAI). At the bottom left of the paper, it states the work was done in 1950 at the USDA facility. Lawrence O. Mott was also very involved with the tick program and attended conferences on Anaplasmosis. Therefore, it shows Traub was working with USDA officials and at their facilities working with one of the USDA officials (L. O. Mott) who was involved with the tick programs:

Michael C. Carroll, author of Lab 257: The Disturbing Story of the Government’s Secret Plum Island Germ Laboratory shows that Plum Island sources had discussed seeing pictures of Traub pointing to the sections of the island where he had released ticks for insect simulant tests:

A source who worked on Plum Island in the 1950s recalls that animal handlers and a scientist released ticks outdoors on the island. “They called him the Nazi scientist, when they came in, in 1951 – they were inoculating these ticks,” and a picture he once saw “shows the animal handler pointing to the area on Plum where they released the ticks.30

They said they were rearing infected ticks at the time, and although I failed to make this connection in my book, its recently become apparent to me that Traub may have been selling American biodefense on the idea that these Russian-doll cocktail infected ticks could have served as vectors to inoculate the population with a live bacterial vaccine for poultry, livestock, and humans against a multitude of different foreign diseases. He was back and forth between Colombia in South America and the Northeast United States from 1949-1952,31 loosely in parallel with the bird migration patterns.32

We know Erich Traub was intended to work on arthropod-borne disease since the file for his German female lab tech Anne Bürger proves it as she was to maintain rickettsial pathogens in serial passages:

Duties of the position to be filled by Miss Burger are concerned with the supervision of maintenance of approximately 40 strains of virus and rickettsias [sic] in serial egg and animal passages in order to provide stocks of infectious materials for experimental work in [the] virology division and other divisions of the Naval Medical Research Institute.33

It also proves they were the most skilled at what they were doing and no one else had the sophisticated level of skill and understanding that Traub and Bürger had:

In view of past long association in the fields of bacteriology and virology with Dr. Erich Traub, whom she will assist at the Institute, Miss Bürger’s assignment here cannot be as adequately filled by any personnel available in the United States.34

In fact, there were no top-rate scientists in America that could replace them and Traub himself was the most prized scientist in the global biological weapons race:

Dr. Traub is an eminent virologist and an authority on matters pertaining to biological warfare. His assignment to the Naval Medical Research Institute will fulfill an urgent need that cannot be met by personnel available in United States. His probable knowledge of preparations for biological warfare in other countries renders mandatory every effort to secure his services.35

Traub was listed as a supervisory bacteriologist in his intelligence file, so he was clearly overseeing simulant tests, routine at the time and which were learned from being advised by the Nazis in Paperclip since that’s how they ran their biodefense program, and most likely the simulant tests were a covert vaccination program using open-air germs and insect vectors like ticks and mosquitoes. We have the source in Lab 257: The Disturbing Story of the Government’s Secret Plum Island Germ Laboratory discussing the section of the island where Traub was said to be releasing the ticks, but we also have a later publication showing abandoned tires still dotted the landscape from earlier tests on the island in a survey conducted and published in a 1980 issue of Mosquito News, “Aedes atropalpus Breeding in Artificial Containers in Suffolk County, New York.”36

What makes me think Traub may have been selling the tick and mosquito simulants as a vaccine program is because he used to refer to immune tolerance as infectious immunity and the multiple overlapping infections produce exactly that.3738 In my book I talked about how Vaccinia virus was cleared as a standard simulant to be used in open air tests by the 1950s,39 and back in 1940 Erich Traub gave the simulant bacteria Serratia marcescens properties of bovine papular stomatitis virus, a poxvirus very closely related to Vaccinia.40 In the 1990s, these simulant tests were still going on, and it makes no sense to continue spreading bacteria in open-air tests for decades “just to see how it spreads out.” It makes more sense as a covert vaccine program done routinely without our knowledge or consent, and indeed they were looking at what vaccine viruses could be used as standard simulants by the 1990s.41

In 2012, NIH was still trying to sell the idea of immune tolerance as a defense strategy,42 which indicates that they were looking at immune tolerance as an acceptable immunity all along since the days of Traub, just as today we are talking about vaccinating the population with mosquitoes released into the environment.43

Plum Island Was Chartered to Handle Foreign Animal Diseases like Lyme Disease and its Co-Infections, so Why Didn’t They?

Plum Island was chartered to study not just FMD but all foreign animal diseases that affected poultry, livestock, and man. Rachel Verdon’s book Lyme Disease and the SS Elbrus claims that after talking to former Plum Island director Dr. Roger Breeze about whether Plum Island was involved with the Lyme disease outbreaks in America, he adamantly told her it was not true, that they never worked with spirochetes or tick-borne disease, and she believed him.44 We can see that such a statement is actually a blatant lie - they published a 1961 paper on subclinical Leptospirosis of cattle.45 Leptospira is a spirochete and Plum Island did work with other tickborne diseases like heartwater (Cowdria ruminantium) and Theileria parva.46 There was a notable paper on early Lyme cases isolating Leptospira spirochetes from the bullseye rash of Lyme patients, and they ignored its significance because it did not produce a robust antibody response, which would be expected since Leptospira is very immunosuppressive.47

Dr. Breeze also told Jesse Ventura in an episode of Conspiracy Theory that he did not know who Erich Traub was when asked.48 This would be inconceivable as anyone with deep experience in the field of virology and FMD virus would have known who Erich Traub was, especially since Roger Breeze was a former roommate of Robert Shope, the son of Traub’s American mentor who had dinner with Traub in the late 1970s.49 This is telling because it shows defensive behavior and intentional dishonesty coming from the director of Plum Island toward anything related to Lyme disease, tick-borne disease, and Erich Traub.

But what is more telling than the intentionally misleading statements is why Plum Island didn’t take any interest in Lyme disease and its co-infections when the outbreaks began happening right in their backyard - since those types of foreign animal diseases were exactly the kinds of diseases that Plum Island was set up to handle and put study into.50 It shows serious incongruency and such anomalies need explaining. It would be like if a shootout happened in a certain jurisdiction and the police just left it for the town hall to deal with.

This is especially noteworthy since several top Plum Island officials had attended the earlier 1953 poultry conference on biowarfare on the poultry industry discussing avian spirochetosis as an agent of special concern.51 It stated that they believed several foreign animal diseases had already gained entrance into the U.S. and a bioterrorist using multiple overlapping infections in the same host was one method that could be used against them, exactly what Traub was doing. Lyme disease is carried by a multitude of birds and can affect land animals, and that makes the safety of the poultry industry a clear and present concern.

From the early 1950s to the 1960s there were several outbreaks of Borrelia anserina across the United States, and in one paper on an outbreak in Arizona from 1960 thanks William Hinshaw of the Fort Detrick U. S. Biological Warfare laboratories – which shows that biowarfare specialists had a clear interest in this pathogen.52 Especially noteworthy are the attempts to study its “carrier state” in chickens,53 and in the immunosuppressed.54 Were they expecting it to suddenly turn from a highly fatal disease to an avirulent pathogen? What would give them that idea? Was it because Dr. Traub had been selling them on the idea of immune tolerance as a vaccine to impart an infectious immunity? That he could make an avirulent vaccine strain of Borrelia anserina mixed with other foreign tick-borne diseases which he could then use in the insect simulant program as both a tracer and a vaccine?

These simulant tests appear to have continued all the way up to the present day as an integral part of biodefense activities. There is no evidence to suggest they ever stopped. Interestingly, a document from the early 90s shows they were not only still assessing what pathogens they could use as standard simulants, they were looking at what vaccine viruses they could use, lending more weight to the simulant program being a covert immunization program done without our knowledge or consent.55 Calling it a standard simulant implies it is routinely done, and surely they would have figured out the dynamics of “how it spreads out” by the 1950s, but this was a probably just a cover to hide the fact they have been attempting to immunize us without our knowledge or consent all this time.

Despite adequate backlash by concerned citizens about the human rights violations that occur by testing on the population without their knowledge or consent, the government still struck these concerns down and ruled that the tests were indispensable to biodefense. The fact that Vaccinia virus was cleared as a safe simulant in the 1950s yet excluded by the 1990s due to its dangerous potential shows the gap in safety assessments:

1950s:

UK outlined the work done on vaccinia, emphasizing that this was very much an interim report. Because vaccinia was relatively safe, easy to produce and easy to assess, it was used as a simulant in both laboratory and field trials in order to gain in formation on the use of smallpox virus (Variola) as a [biological warfare] agent.56

1990s:

Despite its extensive use for immunization of the human population against smallpox, vaccinia virus is a virus of relatively high pathogenicity with a long, if sporadic history of lethal infections and postvaccinial encephalitis. Even more serious than the standard complications listed in the Submission is the prospect of vaccinial pneumonia in a population now almost devoid of the individual or herd immunity resulting from smallpox vaccination. Vaccinia virus must unquestionably, therefore, be excluded.57

I wonder how many injuries or deaths had to occur before they realized the shortcomings of their earlier assessment that it was safe? This re-assessment from the 1990s was also looking at new live agents and vaccine viruses that could be used as standard simulants and serve as replacements to Vaccinia, citing poliovirus, Newcastle disease Virus, measles, mumps, and rubella. This is highly alarming and erodes the fabric of basic human freedoms that we should have a say in.

After learning what immune tolerance is and how it destroys health, brings neuropsychiatric disorders, and cancers, it is beyond criminal to remove someone’s right to be free from such health-destroying agents unleashed upon us without our knowledge or consent. It totally undermines the idea of a free society, of bodily autonomy, of informed consent. It puts us back in the conditions of Nazi Germany and the Soviet Union.

Subclinical Leptospirosis in cattle being studied by Plum Island Animal Disease Center shows they were probably conducting testing with live bacterial vaccines that induced immune tolerance as an infectious immunity rather than the so-called sterile immunity where the pathogen is cleared. This infectious immunity, or immune tolerance, comes with serious long-term often irreversible side effects and poor quality of life in the future. It also comes with death via cancer and wasting disease – an indirect but more painful and agonizing way to die since it is so prolonged and slow.

Traub probably got full approval by American biodefense to conduct these tests if he was selling them on the idea of disease tolerance as a form of immunity. This would indicate he was rearing these ticks with multiple pathogens as live bacterial multi-valent vaccines. In 1961, they were putting forward the idea of using immune tolerance in vaccination campaigns to keep the poultry industry afloat.58 Even in more recent times (2012) they were still trying to sell disease tolerance as an acceptable form of immunity.59 We have obviously learned nothing from the harm caused by the simulant program. Now they are probably trying to create vaccines to protect against earlier “vaccines.”

However, not to get too far off track, my point in discussing this activity in America is to show that highly sophisticated conditions for multiple pathogens in tick vectors would have been once again at play on the North American continent, and Traub’s work on adapting FMD to chicken eggs showed that antibacterial resistance was an environment Traub was familiar working in when he mentioned that certain bacteria contaminated his FMD experiment and survived heavy doses of Streptomycin and Penicillin, and this may have been done intentionally.60 He could have adapted Borrelia burgdorferi to such environments making its 16S rRNA operon highly mutable to change, making what seemed like entirely new species and subspecies between the other European and Japanese forms of Lyme disease when in fact it was still an outgrowth of what had started with a single species - Borrelia anserina - in 1939. He would have completely remodeled the spirochete perhaps several times over in his work on high-density pathogen-packed ticks released in variable ecosystems in routine biodefense activities spanning the globe.

Literature on Borrelia anserina is extremely limited compared to Borrelia burgdorferi, and no sequencing of the spirochetes or any other co-infecting pathogens maintained by Schäfer, Traub, or Beller from that time were ever conducted. Add this to the complex, sophisticated environments they were placed in. Conditions, fair to say, that have never been considered as man-made bioengineering and directed evolution. They found all these species in the Lyme clade and no one can say with any certainty that these aren’t very recent events considering the global spread of the pathogen.

Because of Horizontal Gene Transfer (HGT), chimerism, and the complete absence of modern ethical open source studies to replicate the high-density, multi-pathogen, bacteriophage and mycoplasma-facilitated cocktail in the Ixodes or other ticks across vastly diverse climates has never been considered in the construction of phylogenic trees by academic researchers. It shows us that standard phylogenetic trees do not necessarily account for the very sophisticated man-made influences at work. This would be especially true regarding the Lyme Borreliosis clade having descended from Borrelia anserina as a very recent event, undergoing rapid evolution in a short time frame, across multiple points of the globe, each with their own unique ecosystem, creating what appears to be long-term evolutionary distance spanning millions of years between the evolution of new species, when in fact it was just several years of sophisticated man-made evolution.

When comparing Borrelia burgdorferi to Borrelia anserina as a whole, that is, the morphological characteristics, genetic similarities, and host compatibility, the two are in fact extremely similar. Morphologically speaking - in size, shape, and ultrastructure - They both exhibit comparable lengths (roughly 8–21 μm), wavelengths (1.7–3.0 μm), diameters (0.22–0.38 μm), pointed ends, and flagellar arrangements (typically 7–11 sheathed flagella with similar surface-layer architecture).61 Taken together with the presence of the highly conserved flagellar epitopes shared between Borrelia anserina and Borrelia burgdorferi,62 and the fact that birds serve as immune tolerant carriers of Borrelia burgdorferi,63 this reflects very close relationships, far more powerful than relying on the phylogenic tree alone as a deciding factor. Especially when we add in all of the manmade elements that would have contributed to the rapid evolution of Borrelia anserina brought to many corners of the globe and packed into ticks with multiple overlapping co-infecting agents, mycoplasma, viruses, and bacteriophages.

From the 1995 paper by Hovind-Hougan discussed above on A morphological characterization of Borrelia anserina, clearly comparing Borrelia burgdorferi to Borrelia anserina showing striking similarities:

But Richard Marconi had in fact put forward in his paper that the Lyme Borreliosis clade descended from Borrelia anserina, which served as an outgroup. If Traub and other colleagues (whether Germans, Russians, Americans, Iranians, and so on) had been restructuring the spirochete for multi-system changes such as interspecies transfer or adaptation, changing tropisms, and giving it highly unusual growing environments like the Russian-doll cocktail of overlapping infections in a single vector, with additional horizontal gene transfer through mycoplasma and bacteriophages to shuttle a sophisticated network of genes between the agents, this new clade would be exactly what one would expect to see.

The fact that all the way up to 1951 the black-legged tick was not listed as a transmitter of any known human disease, but then suddenly has multiple overlapping human diseases all rolled into the same vector within a decade is highly unusual. However, if seen through the lens of the story in The Sleeper Agent, it makes sense that they would have began using the black-legged tick for such insect simulant tests, and the USDA was collecting black-legged ticks off animals on a routine basis according to Andrew J. Rogers in his 1951 thesis A Study of the Ixodid Ticks of Northern Florida, Including the Biology and Life History of Ixodes Scapularis Say (Ixodidae: Acarina).64

Therefore, to say that Borrelia burgdorferi and the Lyme Borreliosis clade of Borrelia could not possibly have come from Borrelia anserina in just several years based on the phylogenic tree data alone is jumping the gun and oversimplifying the situation to reflect an assumed natural evolutionary phylogenic tree when quite the contrary is true. These were exceptionally unique and highly sophisticated conditions and environments overlapping that could have easily transformed the pathogen into what seemed like an entirely separate clade - the Lyme Borreliosis clade - and all from one species that was remodelled perhaps several times and continued to undergo rapid evolution on different parts of the globe in the span of just a few years.

Again, I have never claimed absolute proof of every step of the way, I’ve been looking at the big picture and rebuilding the storyline until there are no contradictions. So far the totality of what I present fits the picture exactly without contradiction based on available data, and I present my case as one would do in a court of law, and I believe I have made my case beyond a reasonable doubt which I presented to the public in my book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare.

After schooling Grok on the complexity and sophisticated elements involved in this biological weapons race, the LLM realizes that its responses to Henshit’s questions were lacking and often incorrect, as the LLM’s expertise does not match my own many years of study and it acknowledges its mistakes:

Grok’s advice for Henshit:

Suggested reading

Revisiting bacterial phylogeny: Natural and experimental evidence for horizontal gene transfer of 16S rRNA

https://pmc.ncbi.nlm.nih.gov/articles/PMC3661144/

Phylogenetic classification and the universal tree

https://pubmed.ncbi.nlm.nih.gov/10381871/

Seeing the Forest for the Trees: The Limitations of Phylogenies in Comparative Biology.

https://www.journals.uchicago.edu/doi/pdf/10.1086/660020

Horizontal gene transfer in evolution: facts and challenges

https://pmc.ncbi.nlm.nih.gov/articles/PMC2842723/

Uprooting the tree of life

https://pubmed.ncbi.nlm.nih.gov/10710791/

Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis

https://pmc.ncbi.nlm.nih.gov/articles/PMC2919648/

Identification of novel insertion elements, restriction fragment length polymorphism patterns, and discontinuous 23S rRNA in Lyme disease spirochetes: phylogenetic analyses of rRNA genes and their intergenic spacers in Borrelia japonica sp. nov. and genomic group 21038 (Borrelia andersonii sp. nov.) isolates

https://pubmed.ncbi.nlm.nih.gov/7494041/

Footnotes

For additional commentary, see the video above. The article below also contains an article I wrote back in 2016 called Scopolamine and Mind Control: Intelligence Agencies and the Search for an All-Subversive Agent

(please note: for full article please either read this from the Substack site, or click on “View entire message” in your email and you’ll be able to view the entire post in your email app because if you are reading from email, it will clip some of the message)

I’d like to take some time with this article to resurrect some of my older research that applies to something critical today, since there is so much focus on Jeffrey Epstein, in the hopes of giving some answers to some of the victims of Jeffrey Epstein, as well as just generally informing the public. While my main area of focus is primarily focused on biological warfare, I feel it is necessary to write this article because of my prior expertise of a drug known as scopolamine, a drug that I began researching many years ago. Before I started to go deep into the realm of biological warfare, I had been researching the history and effects of this class of drugs known as tropane alkaloids (atropine, scopolamine and hyoscyamine), synthesized from certain plants in the nightshade family. This drug, scopolamine, comes from the plants Datura, Brugmansia, Henbane, Belladonna, Mandrake, among others of that class containing the tropane alkaloids.

These plants and their alkaloids have a long history going as far back as ancient Sumer and Babylon. I actually mentioned these plants in The Sleeper Agent as a footnote regarding ancient methods of chemical warfare early in the book. It was used in ancient times as a chemical warfare agent, where extracts of the plant would be put into wine or drinking sources of an enemy army and effectively drug them all into a stupor that could last for days, at which time they are easily overtaken and subdued.

Scopolamine is a versatile drug that can be used for a variety of different things. In smaller doses, it treats motion sickness. It is also used in larger doses to induce twilight sleep and has been given to mothers giving birth. However, in these larger doses, and in a more nefarious setting, it has been used by criminals for date rape, robbery, kidnapping, and even murder. Oftentimes when used for these more nefarious purposes the victim will have very little memory of what happened.

I had written about this drug in an article from 2016 on a site I ran about the plants, because of their rich history. They are very beautiful plants and I had been growing them for years, which sparked my interest in researching their history. The plants have been used for such a wide variety of things, not merely for nefarious purposes, but in small doses they can be medicinal, used in homeopathy, and the plants have a long history in shamanism and witchcraft. It was thought that a feminine spirit resides in the plants, so the shamans would use the plants to engage and work with her.

This article I had written, Scopolamine and Mind Control: Intelligence Agencies and the Search for an All-Subversive Agent, was about the use of this drug by intelligence agencies during the early days of MKULTRA. I will republish the information from that article in this post, in the hopes of giving some of the Epstein victims some much-needed answers, especially as it relates to memory loss, among other health problems in which this drug may have been used and contributed to.

I have come across information by Epstein victims suggesting that they were drugged with scopolamine. It does not seem to have been done on every encounter, but it seems to have been done on certain occasions and for very select purposes, especially if the women were being used in government black projects like the harvesting of their eggs and things of that nature.

The effects of the drug, depending on the dose, can last for many hours to days. However, when it is given on enough occasions it can have long lasting effects that linger for a very long time, including memory loss, forgetfulness, absentmindedness. It can also cause psychiatric problems and hallucinations and vision problems that can linger for months or years. When under the effects of this drug, it can also alter the perception and scenery around them via hallucinations. So, a lamp may appear as an animal or something entirely different than what it actually is, other times it has been reported that people appear to them that are not actually there and see things that are not there.

Teenagers have been known to experiment with plants containing the drug because of its hallucinogenic properties, and the hallucinations can seem entirely real. For example, here is an example of some of the hallucinations seen by those who took large doses of the drug from plant material, these are trip reports from erowid.org:

“I looked at the foot of my bed and my two best friends were standing there. I started laughing hysterically at the fact that they would stop by and wake me up at such a late time. I preceded to have a little party in my room with them. They came up and sat on either side of me and we had a great time passing joints and smoking cigarettes. I paused the little shindig and went to the bathroom. I used the bathroom and while washing my hands I looked into the mirror and my face contorted into an impossible shape and I shook myself off and splashed some water on my face, still none the wiser to what was happening. I walked back to my room where at my door my mother was standing. I greeted her and informed her that my friends had stopped by for a late night visit. She gave me the weirdest look I think she has ever given me. I re-entered my room and my friends were nowhere to be found.”

Other times more unusual hallucinations can occur:

“I’ve been seeing this giant spider run around in circles in my livingroom. Everytime I get near it, it hisses at me. It’s started to freak me out.”

It was being used by intelligence agencies and at Guantanamo Bay after 2001, where an Australian journalist was once held as a prisoner and he was given injections of scopolamine. They told him it was for motion sickness, but it is highly unusual to give injections of it for motion sickness when it can be delivered in a patch placed behind the ear, as is the usual method for delivering scopolamine for motion sickness. It was more likely injected into this prisoner because the drug is also used as a truth serum and is the actual truth serum that the CIA found, it was not LSD as most people think. Scopolamine is a mind control drug and a truth serum. Wikileaks released a talk by a Dr. Larry Forness of the American Military University lecturing about the drug and he says definitively that scopolamine is a truth serum when injected in the right place, in the right amounts.

But it can also be made into a powder and blown into the face and eyes. It rapidly absorbs into the mucosal membranes and puts a person under the spell of the drug in seconds. Much of what follows will not be remembered, as it acts to block the formation of memories.

Many of Epstein’s victims have reported memory loss. They can’t remember and experience “missing time.” This is entirely characteristic of being drugged with scopolamine. Scopolamine can put a person in a state whereby they have no free will and puts them into a blank state, like a child. Much of what happens during that time will not be remembered upon recovering from the drug because it blocks the formation of memories. It does not mean that they can’t still remember certain things that happened, as flashbacks can occur, but much of it will not be remembered due to this inhibitory effect on memory formation. One of the effects of the drug is an extremely dry mouth, and this may help some of the victims to identify whether they were given the drug. Other symptoms can include blurry vision, and sensitivity to light.

What is rather unusual about this drug is that it can be absorbed through the skin. And in the recent Epstein emails there is an email showing a victim impact statement describing how he was drugged with scopolamine simply by turning a doorknob that had been smeared with scopolamine-laced Vaseline:

“THE VICTIM IMPACT STATEMENT OF DR. JOSEPH MANZARO”

It was about 5:30 P.M. on December 26, 2014. When I arrived home at 424 Valley Forge Road in WPB, I unlocked my door and when I turned the handle on my door, I got something all over my hand that resembled VASELINE! I said to myself, ewe, that’s disgusting. I rubbed my fingers together and my hands as I went in to wash my hands to see what the heck this stuff was?

The next thing I remember was waking up in the backseat of a car and being driven somewhere! It was Eric Mejias driving and Bony Rivera in the passenger’s seat! I said hey guys, what’s going on, where are we going? What am I doing here? Why are we driving anywhere, I’m supposed to be at home right now! Then I said, oh wow, I’m really sleepy. I need to just put my head back a bit okay...

The next thing I remember was waking up again and hearing Bony Rivera telling Eric Mejias that I was waking up! He said “He’s waking up cuz, WHAT should I do?” Eric Mejias then told him not to worry, just give it a minute, he’ll fall back asleep again, I gave him a LOT of that Scopolamine! [HE MUST HAVE GIVEN ME A LOT BECAUSE I AM PRACTICALLY IMMUNE TO THAT STUFF! AS A CHILD I HAD TO TAKE IT QUITE A BIT TO GO DEEP SEA FISHING WITH MY DAD ON THE WEEKENDS WHICH I LOVED! I JUST HATED BEING SEASICK AND DEVELOPED QUITE A LARGE TOLERANCE TO SCOPOLAMINE! I KEPT THAT TO MYSELF THOUGH!] (EFTA00163101)

In another email, a New York based model/fashion photographer Antoine Verglas sends Jeffrey Epstein an article from Vice that had investigated the drug and its use in Colombia, where it is known as “the Devils Breath”:

The most dangerous drug in the world: ‘Devil’s Breath’ chemical from Colombia can block free will, wipe memory and even kill

• Scopolamine often blown into faces of victims or added to drinks

• Within minutes, victims are like ‘zombies’ - coherent, but with no free will

• Some victims report emptying bank accounts to robbers or helping them pillage

own house

• Drug is made from borrachero tree, which is common in Colombia (EFTA00865569)

I will now include and republish my older 2016 article for more in-depth information about scopolamine and its use by intelligence agencies:

Scopolamine and Mind Control: Intelligence Agencies and The Search for an All-Subversive Agent

By: A. W. Finnegan (written in 2016)

In the 1970’s all hell broke loose when an article in The New York Times surfaced about the CIA’s Project MKULTRA human mind-control program. This was a program to study how the human mind can be subverted, manipulated, incapacitated, wiped clean, or exploited as a technique of war. The project was carried out on unwitting civilian test subjects through the use of drugs, hypnosis, sexual abuse, sensory deprivation, and torture. This began in the late 1950’s and carried on through the 60’s and early 70’s. And although they claimed it stopped there, this should mean little coming from the organization that is structured on the art of deception. Almost all of the research and documentation has probably been either hidden away or destroyed lest its crimes exposed and its names prosecuted.

Most of what the public knows about MKULTRA, if much at all, would say “it was about LSD and the search for a truth serum.” but the well-informed members of society and researchers out there understand MKULTRA was a covert mind-control program that sought about exploiting and abusing unwitting citizens to produce effects and actions against the will of that individual, against the law of the land, and in certain times even at the cost of life itself.

MKULTRA experimentation was carried out in many facilities across the United States, but some of the most inhumane experimentation happened on Canadian soil, at the Allen Memorial Institute, in Montreal. Headed by a Dr. Ewen Cameron, a prestigious Psychiatrist and at one time a president of the American Psychiatric Association. Many of the unwitting participants had checked into the hospital for something treatable, only to have their whole life destroyed and forever traumatized by these horrific experiments.

From a little research utilizing the extensive literature out there on MKULTRA, with similar programs like ARTICHOKE, MKOFTEN, MKDELTA, and its many other names, it is clear that their interest in drugs mainly had to do with isolating and fine tuning substances for such uses as:

A) Subversion/Mind-control

An agent that could create the highest suggestibility, having a subject without question act in a way contrary to his/her individual will, against their own safety, and preferably hidden in a state of amnesia upon awakening.

B) Incapacitating Agent

An agent that could completely incapacitate one from performing duties or daily activities from anywhere from hours to days.

C) Truth Serum

An agent that could create a state where the ability to lie is not withstanding and the known information is withdrawn accurately without much effort.

The full spectrum of the avenues covered by drugs in mind-control programs were listed as:

1. Substances which will promote illogical thinking and impulsiveness to the point where the recipient would be discredited in public.

2. Substances which increase the efficiency of mentation and perception.

3. Materials which will cause the victim to age faster/slower in maturity.

4. Materials which will promote the intoxicating effect of alcohol.

5. Materials which will produce the signs and symptoms of recognized diseases in a reversible way so that they may be used for malingering, etc.

6. Materials which will cause temporary/permanent brain damage and loss of memory.

7. Substances which will enhance the ability of individuals to withstand privation, torture and coercion during interrogation and so-called “brain-washing”.

8. Materials and physical methods which will produce amnesia for events preceding and during their use.

9. Physical methods of producing shock and confusion over extended periods of time and capable of surreptitious use.

10. Substances which produce physical disablement such as paralysis of the legs, acute anemia, etc.

11. Substances which will produce a chemical that can cause blisters.

12. Substances which alter personality structure in such a way that the tendency of the recipient to become dependent upon another person is enhanced.

13. A material which will cause mental confusion of such a type that the individual under its influence will find it difficult to maintain a fabrication under questioning.

14. Substances which will lower the ambition and general working efficiency of men when administered in undetectable amounts.

15. Substances which promote weakness or distortion of the eyesight or hearing faculties, preferably without permanent effects.

16. A knockout pill which can surreptitiously be administered in drinks, food, cigarettes, as an aerosol, etc., which will be safe to use, provide a maximum of amnesia, and be suitable for use by agent types on an ad hoc basis.

17. A material which can be surreptitiously administered by the above routes and which in very small amounts will make it impossible for a person to perform physical activity.

Historically, I will point out that scopolamine has been employed to carry out most if not all of these agendas in some form or another at differing times and places, long before the CIA began its infamous mind-control program at the start of the Cold War.

Part I: secrets on the outside

From the earliest of times, the tropane-based nightshade plants have been used in chemical warfare, and criminal poisoning to manipulate or greatly reduce a target’s ability to function in that setting. In the past, soldiers from other armies would be lured into drinking wine laced with henbane, mandrake, or deadly nightshade, only to be left wandering about as rambling, incoherent idiots. An example of this being Antony’s Army in the Parthian Wars. These nightshade plants (Solanaceae) were some of the earliest known forms of chemical warfare and poisoning used in the fine art of war.

the tropane alkaloids (atropine, scopolamine, hyoscyamine) have an extremely versatile role in cultures worldwide. They can heal the body of everyday ailments, they can ease suffering, they can be used for deep sleep in painful situations like bone-setting, and they can also kill. As they were used for spiritual and divine purposes by the shaman and witch-doctor alike, they were also used to carry out dirty and deceptive deeds as well.

On the one hand, someone could argue that the tropanes are far too incapacitating with too many nasty side effects that make it difficult to work on a subject. The ‘delirium’ would make one uncooperative, irrational, and full of nonsensical communication. Nothing could get done, and would be shrugged off as useless…

On the other hand, could the delirium be reduced and controlled by dosage while also bringing through the submissive, zombie-like state that renders one capable of control? Could it be possible for someone to have you drugged, take control and coerce you into actions against that which you would ever think to do otherwise while in this state? With such high suggestibility the subject could be extremely malleable. Taking control of such an individual would not be so out of question.

One thing to consider among the use of tropane alkaloids like in application for use in a military setting, there are over 500 variations and derivatives of the original 3 most known tropanes available from the plant material. With this in mind, fine tuning the substance has probably had an amazing run in a classified setting, with plenty of time to get it right.

In Latin American culture, the criminal use of scopolamine is a real threat to many ordinary people living there. There are reports of people unwittingly swept under its spell by drugging and will empty their bank accounts, give all their furniture away, bank account numbers, credit cards, anything of value, and wake up with no memory of what happened.

In one case there was a woman in Bogotá, Columbia who last remembers riding a city bus with her newborn baby. Three days later she awakens in a hospital after being found badly beaten and wandering around topless on the median strip of a busy highway. “When I woke up in the hospital, I asked for my baby and nobody said anything. They just looked at me.” Her baby was nowhere to be found. Police believed that she was drugged with scopolamine and her baby was taken by gang members involved in the trafficking of infants.

It might be hard to believe that a mother would actually give up her baby to strangers. But under the spell of scopolamine it can happen very easily. This is because once the confusion takes control she is immediately thrown into a state similar to a blackout drunk. She is unaware of her present life, what she was just doing, where she was going, who she was with, who is a danger from who is not. They may ask her to hand over the baby, and while obliviously handing him over she is unable to connect the dots that she is actually giving away her own child. As she is not able to rationalize or account for her actions and responsibilities, she cannot see the gravity of her situation either- That her son is out of her arms and gone forever. The same can be done for robberies or date rape, and it is a drug that can be used for extremely nefarious purposes.

Scopolamine also made headlines in the 1920’s as a ‘truth serum’ when a man by the name of Dr. Robert House, an obstetrician, discovered scopolamine as a means to extract information out of people. He was very much opposed to a criminal’s constitutional rights being used to cover his tracks and thought this would be the glue to getting more convictions and letting go of those who were falsely accused but actually innocent. Scopolamine was the answer. As he stated in his some of his articles concerning scopolamine:

“Scopolamine will depress the cerebrum to such a degree as to destroy the power of reasoning. Events stored in the cerebrum as memory can be obtained by direct stimulation of the centers of hearing.

My attention was first attracted to this peculiar phenomenon September 7, 1916, while conducting a case of labor under the influence of scopolamine. We desired to weigh the baby, and inquired for the scales. The husband stated that he could not find them. The wife, apparently sound asleep, spoke up and said, ‘They are in the kitchen on a nail behind the picture.” The fact that this woman suffered no pain and did not remember when her child was delivered, yet could answer correctly a question she had overheard, appealed to me so strongly that I decided to ascertain if that in reality were another function of scopolamine. In a confinement case you find your dosage by engaging the patient in conversation, to note the memory test. Hence my investigation was a simple matter. I observed that, without exception, the patient always replied with the truth. The uniqueness of the results obtained from a large number of cases examined was sufficient to prove to me that I could make anyone tell the truth on any question.”

All this is very telling because thus far we are able to ascertain how a drug like scopolamine can:

A) Induce a state where the victim will give anything away, even her most precious baby boy, without having any misgivings about it at the time. Without rationale or thinking of consequence.

B) Act on the brain in such a way that when under the influence of scopolamine the subject is unaware of the need to deceive, and likely to respond truthfully with what they know in regards to a question asked.

Understand that these two characteristics make a perfect setting for control of the mind and it has already displayed a wide spectrum of application long before the official search for such a drug began in Project MKULTRA. Perhaps the LSD was not the main attraction within the walls of MKULTRA but used as a red herring to move attention away from their perfecting of scopolamine.

Part II: secrets on the inside

Unfortunately, because of the nature of classified information, and especially so with the Central Intelligence Agency, much of what took place in project MKULTRA, MKDELTA, MKNOAMI, MKOFTEN, MKSEARCH, ARTICHOKE, and the rest of the mind-control operations of the early days of mind control have thankfully been somewhat pieced together by whistle-blowers and researchers, gathering statements and letters written by personnel, documentaries, scandals, lawsuits, and victim testimonies. The truth of the matter is that hardly anything came to light from FOIA requests and what little did was almost certainly ‘damage control’ geared towards refuting any progress made as ineffective and inconclusive.

On top of that, Many of the actual files and secrets of CIA mind-control operations have been destroyed as scandal came to light before the Church Committee of the U.S. Congress in 1975. The nature of what took place to procure the results was as criminal as it was inhumane.

Drugs like LSD, PCP, and various other psychoactive substances all played a part in forming a database and recipe book on the manipulation of the human mind as far as drugs are concerned. But as far as a single substance capable of such nefarious purpose and complete subversion of the human mind is concerned, scopolamine is the elite.

The concept of creating a ‘Manchurian Candidate’ assassin has been brought up again and again throughout the last few decades. This was using torture, drugs, and hypnotic suggestion to create a killer to be used later on activated by triggers, being words or actions to activate hypnosis. I will not tread too deeply in this direction other than to say that it is certainly reasonable to assume its possibility. Given that hypnosis is truly an art of its own, and on its own gets results. The CIA would have most certainly employed the best of the best in hypnotists. When combined with the addition of drugs and torture in a person affected by Post Traumatic Stress Disorder, it would certainly be a plausible scenario.

MKOFTEN was the joint venture of the Department of Defense and CIA’s covert operations into the Occult and employed a high number of men and women skilled as black magicians, satanists, sorcerers, clairvoyants, palm-readers, fortune-tellers, astrologists, psychics, mediums, demonologists, witches, warlocks, and other Occult-practitioners. There have been a number of African Traditional Religions religions as well as European and Indian practices that use tropane alkaloids in their systems.

The mind-control/subversion aspect of scopolamine is pretty straight forward. In Latin America, it has already been displayed on a massive scale in criminal activity and hospital staff are well aware of this fact. The induced confusion and invasive stupor caused by this compound renders one extremely docile and childlike in ability to withstand outside influence. Understanding how the CIA utilized it is not so much about reading actual declassified documents as it is ‘connecting the dots’ from other people and places using it for such nefarious means. In other words, criminals have already been using it for all of the purposes that the CIA were looking to achieve with a single substance.

James S. Ketchum, M.D., Author of Chemical Warfare: Secrets Almost forgotten, gave us some invaluable information on some of the ways these compounds work because of his time working in chemical weapons for the ARMY in the 50’s and 60’s testing a synthetic atropine-derivative called 3-quiniclidinyl benzilate, or simply, BZ. Atropine is similar to scopolamine. Unlike MKULTRA, this was a voluntary ARMY program where soldiers could test out drugs or chemicals for the ARMY in a controlled setting with medical staff in return for certain perks and benefits like being able to spend time closer to family and such. BZ was given to soldiers who volunteered to be used as test subjects at Edgewood Arsenal, Maryland in the 1960’s. They were not told what they would be given since it was Classified at the time. When testing out BZ they would be in a deep stupor for about 72 hours.:

“In reality most volunteers did not consider incapacitation with BZ to be a seriously unpleasant experience, as long as good nursing and medical care was provided. It was pretty much like a lost weekend – 2-3 days of drunkenness, but quickly forgotten. Surprisingly, many described a feeling of well-being following recovery. Both men were quite willing to repeat the test (another illustration of voluntary as opposed to “unwitting guinea pig” participation)”

There is a chapter in Ketchum’s book in the beginning where he goes over some of the history of the solanaceous compounds being used to incapacitate people in early wars before technology became so prevalent. A very important look at how these compounds have been used as incapacitating agents in ancient and modern times.

As far as scopolamine as ‘truth serum‘, Dr. House paved the way for such invasive means of getting it out of a person, which then went on to be used by some law enforcement back in the day. The CIA was well aware of this fact, as it was presented in declassified documents. Here was the reason they knew to find it in this particular avenue. But of course, we are told it was a dead end street. In one declassified document detailing scopolamine as ‘truth serum‘, the conclusion states:

“Because of a number of undesirable side effects, scopolamine was shortly disqualified as a ‘truth’ drug. Among the most disabling of the side effects are hallucinations, disturbed perception, somnolence, and physiological phenomena such as headache, rapid heart, and blurred vision, which distract the subject from the central purpose of the interview. Furthermore, the physical action is long, far outlasting the psychological effects. Scopolamine continues, in some cases to make anesthesia and surgery safer by drying the mouth and throat and reducing secretions that might obstruct the air passages. But the fantastically, almost painfully, dry ‘desert’ mouth brought on by the drug is hardly conducive to free talking, even in a tractable subject.”

However, this is entirely contradiction by documents released by Wikileaks. In 2007, a lecture by Dr. Larry Forness of the American Military University surfaced on Wikileaks on Terror, Interrogation, and Intelligence. This lecture “explains the rationale behind torturing prisoners, torture methods, and a justification for ignoring international law. Forness advocates the injection of truth serums, threatening to inject Muslim prisoners with pigs’ blood, and torturing detainees’ friends and family.” The most effective substance in procuring the truth from a subject? Scopolamine. As he describes and corroborates how the declassified document above amounts to complete horse shit:

Fallacy #4. These things called “truths serums” don’t really work.

They do work to varying degrees of success.

There are three primary truth serums.

Here they are.

Scopolamine (scopolamine hydrobromide; first word pronounced: skoh-PAW-lah-mean), also known by another name — hyoscine (hyoscine hydrobromide). It is colorless, odorless and tasteless. Its clinical uses are primarily as a sedative, and applied locally (directly) as a mydriatic, which causes the pupil of the eye to dilate. When used as a sedative, the primary uses are to combat vertigo and motion sickness. When used with morphine and pentobarbital, to a woman in labor, it produces a “twilight sleep.” It is also used as a premedication preliminary to surgery anesthesia.

Since scopolamine completely blocks the formation of memories, unlike most date-rape drugs used in the United States and elsewhere, it is usually impossible for victims to ever identify their aggressors (or interrogators, if you were a prisoner).

To use scopolamine most effectively to get a prisoner to tell you what he or she knows, the key is where you inject it, and in what amounts. Normally it is introduced into the body by a transdermal patch or intravenously in the arm. However, if you inject it into the spine (amount classified), it causes absolutely incredible pain, accompanied by violent convulsions and seizures. If injected into the spine in the appropriate amount, more than 95% of all prisoners will tell the truth — not something fabricated to stop the pain — within 24 hours (Source: classified).

A far milder form of psychological abuse involves exposing prisoners (intravenously or orally) to sodium pentathol—commonly known as “truth serum.” Sodium pentathol is an ultra-short-acting barbiturate that depresses the central nervous system, slows heart rate, and lowers blood pressure. In the relaxed state produced by the drug, subjects are more susceptible to suggestion and are therefore easier to interrogate. The drug does not actually guarantee that prisoners will tell the truth, however. Often, it makes subjects “gabby” without revealing any important information.

Sodium amythal, also known as a type of “truth serum,” with its clinical application in psychoanalysis, is used primarily to help in memory recovery and dealing with “false” memories. If you can confuse the prisoner as to what is a real memory and what is a false memory, you might be able to crack their resistance to telling the truth. However, if the prisoner is smart, he or she will simply shut up and you’ll get nothing from them.

What is interesting is that a prisoner could have been subjected to a truth serum singularly, or two or three over enough time given the appropriate washout of the prisoner’s system, and flatly state that he or she did not tell his or her interrogators anything. From his or her perspective, he or she is telling the truth — because he or she has no memory of telling interrogators anything. That’s the truth in his or her own mind, but it is not the fact of the situation.

In terms of training individuals to resist the three aforementioned truth serums, it is easiest to train someone to resist the sodium amythal, followed by sodium pentathal. There is no known training that will allow anyone to resist scopolamine, when injected into the spine in the correct amount.

What you don’t want to do is “stack” scopolamine with sodium pentathal and sodium amythal. “Stacking” means adding one drug on top of another before the previous drug(s) has/have washed out of the system. You stack on somebody, you’ll kill them.

When time is not a consideration, and when used in conjunction with skilled interrogators on a prisoner who has not been trained to resist the effects, sodium pentathal and sodium amythal will get you the truth in approximately 10% to one third of the cases. When the truth absolutely positively has to be there within five days, forget them – use scopolamine injected into the spine.”

This is corroborated by both a book and an article written about a detainee at Guantanamo Bay, David Hicks. In this article, US use of Truth Drug Revealed, states:

New evidence has emerged that all Guantanamo Bay detainees, including David Hicks, were drugged involuntarily with a substance that has a long history as a truth serum.

Recently declassified US documents revealing medical procedures have shown that scopolamine was administered to all detainees taken to the Cuban detention centre.

The documents, which were standard operating procedures for nursing staff, were obtained by the independent US news outlet Truthout, and reveal that the rationale for the drug’s use on all detainees was to prevent motion sickness.

However, US military experts have said that scopolamine is not recommended for motion sickness because of its severe side effects.

Later in the article where the most telling line in corroboration to the Wikileaks lecture by Dr. Forness appears:

He said it was administered by injection, not a patch behind his ear as is described in the standard operating procedures.

It is wildly out of proportion and unprofessional for a medical team to be treating motion sickness with scopolamine injections. It would cost more and would not be as helpful as a patch that allows for continued delivery over the course of a few days.

Another Source confirms Forness’ lecture and using scopolamine for torture and interrogation:

“The amount of Scopolamine necessary is a minute amount. I am an ex U.S. Army Chemical Core officer and we handled the hazmat on this substance. With proper coercion the amount necessary is between 10 and 20 MG. This will cause a severe state of stupor and hallucinations. During this time however it is possible to interrogate the prisoner thoroughly due to the lack of there [sic] upper brain function during the time. The time the drug is most effective is between +2:30 hrs to +7:30 hrs.”

I have always gone with the assumption that the bulk of classified work and intelligence research always yields a lot more progress than we are claiming them to be, rather than to just meet our expectations of accomplishing what we thought they would. At the same time, the declassified documents will go as far as to admit what they were working on but to refute it all as a dead end street that went nowhere, much like all of the official reports on MKULTRA and mind control.

But all you really have to do to find out what kind of results were made with scopolamine is to look at the history of scopolamine itself. This is one of the most ancient compounds in medicine. Always kept in the backdrop of society and culture but yet ever present. Such a little known compound but one of the most powerful. One of the most medicinal but one of the most toxic. One of the most telling substances on the globe, yet one of our biggest secrets. How’s that for a paradox?

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After reviewing many of the newly released Epstein files from the archive at the Justice Department, it is easy to conclude that Jeffrey Esptein was heavily involved in the biowarfare and biodefense industry, with his hands all over public health, scientific research, most certainly in bed with Big Pharma, and of course, and partnering with heavy-hitter NGOs like The Bill and Melinda Gates Foundation. In this article we will take a look at just some of those, although this is not exhaustive, as I’m sure there are many more, but time prevents me from exploring everything. So lets begin.

There is much in the emails about synthetic viruses and biology, conferences, startup portfolios, pharmaceutical companies, etc. One article THE DOOMSDAY STRAIN: Can Nathan Wolfe thwart the next AIDS before it spreads? (EFTA02684958) Illustrates the type of scientific minds Jeffrey Epstein was interested in and sought to collect and back with funding. He then began to embed himself into the industry, science, medicine, and biodefense, even assisting top NGOs like the Bill and Melinda Gates Foundation.

In one email from The Bill & Melinda Gates Foundation advisor Boris Nikolic, he and Jeffrey Epstein discuss bioengineering to make synthetic biology and viruses, exploiting technologies that operate without regulatory framework, speaking bluntly on the inevitability of accidents occurring and the feasibility of the manufacture of lethal weapons:

But not to fear, because once a pandemic situation unfolds, Jeffrey Epstein and his friend Bill Gates will be there to plan and roll out vaccines and biosecurity strategies while making a lucrative profit, finding ways that circumvent transparency:

This would be Epstein’s strategy - becoming a playbook scheme for responding to pandemics by consolidating wealthy billionaire capital under a single umbrella that bypasses transparency. More to the point, he and his billionaire philanthropists were setting up sophisticated strategies to monetize pandemics through hidden financial channels. In one email to Bill Gates, they discuss pandemic simulations:

He would then work with technical experts high up in intelligence, such as Dan Dubno, who has connections to DARPA and National Defense, and could deliver a pitch for these systems as critical to American Biosecurity policy. Other emails describe pandemic simulations and outbreak scenarios. Clearly, Jeffrey Epstein was knee-deep in the biodefense industry.

Dan Dubno also sends Epstein an article in 2009, Bioterror Failures Criticized, about Obama’s failure to address the threat of bioterrorism (EFTA02438859). In another correspondence, Dan Dubno emails Jeffrey Epstein with the following suggestions on biodefense preparedness and planning discussing an outline for these “deliverables” :

Jeffrey Epstein appears to have been advising Bill Gates associate Boris Nikolic on how to approach disease, in an email to Nikolic from 2009 telling him to look at disease in terms of algorithms:

In an email to Mary Erdoes, investment manager and executive from the JP Morgan asset and wealth management division, Epstein is discussing R & D (research and development) and vaccines:

Mary replies:

Epstein responds:

From as far back as 2003, The Jeffrey Epstein Foundation VI was funding and “established the Program for Evolutionary Dynamics at Harvard University with a $35 million gift to the university. Under the direction of Martin Nowak, the Program is one of the first of its kind to study the evolution of molecular biology with the primary use of mathematics.” From the now defunct Jeffrey Epstein Foundation VI website:

Program For Evolutionary Dynamics

The Program for Evolutionary Dynamics is a graduate department at Harvard University. Under the direction of Martin Nowak, an evolutionist and professor of mathematics and biology at Harvard, the Program studies the evolution of molecular biology with the primary use of mathematics. It is one of the first departments to develop a mathematical model of how cancer cells evolve as well as infectious bacteria and viruses such as HIV. The Program’s models have led to key discoveries towards fighting several diseases. More recently, pivotal work has been done in mapping colon cancer resistance to inhibitor drugs, mapping the progression of pancreatic cancer, targeting the topology of minority mutations that drive tumor growth and creating a database to predict and minimize resistance to HIV drugs. Other current research topics include: evolution of cooperation, cancer, viruses, evolutionary game/graph/set theory, prelife, protocells, eusociality, evolution of construction, population structure, evolution of language, experimental games, and evolutionary economics. Their ambitious goals include curing the world of cancer, infectious disease, selfishness, and inclusive fitness theory.

Additionally, we have discussion to establish a meeting between Epstein and Dr. Ian Lipkin, a top microbiologist/pathologist who would have been a big name in American biodefense and holds expertise in neurodevelopmental, neoplastic (cancer), and autoimmune disorders which is exactly the realm of Erich Traub’s stealth bioweapons that cause immune tolerance, neurodegenerative disease, and cancers:

A significant number of emails had a lot to do with herpesvirus reactivation and the vagus nerve. One email from a redacted source, clearly this is Dr. Melanie Walker, M.D., a neurosurgeon, who was living in Seattle at the time and was married to Steve Sinofsky, emails Esptein about meetings with Bill and a thought about the need to immunize via the vagus nerve:

Steve Sinofsky in 2017, emails Jeffrey Epstein with a link to an article “Bucking FDA, Peter Thiel funds “patently unethical” herpes vaccine trial:”

A 2014 email from a redacted source tells Epstein they should start a lab somewhere to for vagus nerve experiments, , clearly hinting at this being clandestine research:

Even earlier correspondence from 2010 shows redacted sources asking Epstein to fund vagus nerve/herpesvirus research:

It’s a very good possibility that Melanie Walker is the redacted correspondent in most of the emails discussing the vagus nerve and the herpesvirus. For more on Melanie Walker, see article: The neurosurgeon wife of Microsoft exec with ties to Epstein AND Bill Gates: How Melanie Walker met billionaire pedophile who found her ‘very attractive’ before she served as top advisor to Gates’ foundation.

In one email with discussion on the vagus nerve, this redacted source writes to Epstein mentioning herpesvirus reactivation, which was one of Traub’s bioweapon mechanisms:

Epstein then responds with a link to a science daily article which brings us to “Probiotic therapy alleviates autism-like behaviors in mice“ about using a bacterium Bacterioides fragilum as a probiotic to fix autism, but further research on this bacterium as a probiotic led me to “Nontoxigenic Bacteroides fragilis: A double-edged sword“ showing it very may instead cause harm:

Nontoxigenic B. fragilis (NTBF) [...] has been shown to affect the host immune system and interact with gut microbes and pathogenic microbes. Previous studies indicated that certain strains of B. fragilis have the potential to serve as probiotics, based on their observed relationship with the immune system. However, several recent studies have shown detrimental effects on the host when beneficial gut bacteria are found in the digestive system or elsewhere. In some pathological conditions, NTBF may have adverse reactions.

This would align precisely with the overall idea put forward by the end of my book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, where enemies have infiltrated and hijacked our public health system and use it to our detriment. They hijack it and then create practices in policy and preparedness that claim to protect us but actually harm us, and almost no one suspects a thing. Just how Erich Traub attacked the United States in the 1950s under the guise of simulant tests, a biodefense practice whereby a so-called “harmless” bacterium is released in either the environment or in insects and tracked to see how the bacterium spreads out, it is essentially a simulation of bioterror attacks, but in reality, was a bioterror attack.

Epstein victim and survivor from South Africa, Juliette Bryant (follow her onX; https://x.com/JulietteBryant), told me that during the years she was a victim at Epstein’s Little St. James Island, Epstein was meeting with a top ornithologist at the island and considered whether this was possibly about birds being able to spread disease. This exactly what one would expect if Epstein had a hand in biodefense activities, because when Erich Traub was stationed at Plum Island off the Long Island sound in the 1950s, he released ticks infected with Lyme disease and other stealth infections on shorebirds and was travelling back and forth between Plum Island and Colombia in South America, as the military began studying the use of birds to spread biological warfare agents. Little St. James is a small, isolated island is comparably similar to Plum Island, and would have been a perfect spot to continue studies for their avian vector programs to spread Lyme disease and other zoonotic tickborne diseases.

Speaking of Lyme Disease, the recent Epstein files show that Epstein and some of those he associated with understood the neurotropic aspects of these stealth weapons of biological warfare that impart slow wasting diseases such as Alzheimer’s disease and dementia.

One interesting email discussing Lyme disease (Borrelia burgdorferi) and spirochetes causing amyloidosis (wasting disease a.k.a. prion disease) was from a woman running an Alzheimer’s foundation from Switzerland:

In another email from Epstein to someone who’s name is redacted, he makes his connections to expertise on amyloidosis clear:

In another email from a redacted source to Jeffrey Epstein, they are discussing doing experiments, again mentioning the vagus nerve, and in this email the source says to Epstein:

One email was sent to Jeffrey Epstein to take part in a webinar, The Hidden Epidemic of Lyme Disease - Free Webinar, from Dr. Galland’s Pill Advised website, probably because he signed up for the website:

Clearly, Epstein and his associates that worked in biodefense and public health understood the mechanisms of stealth biological warfare – particularly the mechanisms of immune tolerance, virus reactivation, bioweapons that cause neurodegenerative or wasting diseases. In one email to Martin Nowak, Epstein even seems to have a new watchword that describes stealth biological weapons calling it bio-cryptography, and tells Martin to focus on these immunosuppressive proteins which I call the great imitator antigen in my book The Sleeper Agent. He says:

In an email to Michael Sitrick, a prominent figure in Strategic Communications for reputation and crisis management, clearly trying to help strategize with Epstein about propaganda that could be used to elevate Epstein’s image in the wake of sexual abuse and trafficking allegations, Epstein tells him:

In this same email, in response to a question about Epstein’s involvement with charities and prominent figures like the Clintons and Ehud Barak, it shows:

All of the aforementioned correspondence about stealth, virus reactivation, and the amyloidogenic properties of these biological agents goes to show how our public health system has been operating under one set of expertise while telling the public something very different, and have been very dishonest in their dealings with the public, purposely misleading us with public health messaging.

The Bill and Melinda Gates Foundation, for example, had been funding research with NIH to use immune tolerance as a biodefense strategy, in other words, create vaccines that disable the immune system instead of creating an actual immunity, which is an extremely detrimental approach with little to no benefit and comes with severe, even catastrophic long-term health effects like chronic disease, neurological disorders, and cancer. In 2012, some of this research was published as “Disease Tolerance as a Defense Strategy” and listed the funding sources from The Bill & Melinda Gates Foundation, the Howard Hughes Medical Institute, Ellison Medical Foundation, and NIH:

This appears to have been the approach to the COVID-19 vaccines, as the spike protein hits the immune receptors responsible for immune tolerance (TLR2/1, TLR2/6), which is reflected in papers like, IgG4 Antibodies Induced by Repeated Vaccination May Generate Immune Tolerance to the SARS-CoV-2 Spike Protein :

However, emerging evidence suggests that the reported increase in IgG4 levels detected after repeated vaccination with the mRNA vaccines may not be a protective mechanism; rather, it constitutes an immune tolerance mechanism to the spike protein that could promote unopposed SARS-CoV2 infection and replication by suppressing natural antiviral responses. Increased IgG4 synthesis due to repeated mRNA vaccination with high antigen concentrations may also cause autoimmune diseases, and promote cancer growth and autoimmune myocarditis in susceptible individuals.

My book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare tells the story of immune tolerance in the creation of stealth biological weapons that disable the immune system and cause slow chronic disease, neurological disorders, and cancers, which have obviously evolved since the days of Erich Traub, but understanding their history is key to understanding the biological weapons game of today, which is heavily centered on this class of weapons, strategic weapons that tire, exhaust, and overwhelm a target population or country.

Clearly, this is just the tip of the iceberg, but so far, we can see something very ugly about our public health and biodefense with the recent release of the Epstein files, and how a man like Jeffrey Epstein can be so heavily involved in matters of “National Security” should be alarming to many people, as it is a red flag, just like it is a big red flag that the son of a hardcore Stalinist bioweaponeer - Konstantin Chumakov - was running vaccine safety and review at the FDA and approved the COVID-19 vaccine. The evidence is all around us, that our public health system is compromised and needs serious auditing and overhaul. The very system is infested with an enemy force that is working to our detriment and not to our health.

Eye opening aspects of viral contamination of vaccines and the mechanisms of how these viruses creep in, in a dormant state and reactivates later on from immunosuppression, and causes serious chronic disease and cancers

Stealth is a very promising feature in biological weapons work, and it is a sought after characteristic in both the way they spread and the way they act on the host, which by its nature, has to be of the incapacitating agents that slowly tire, exhaust, and overwhelm the targets, rather than cause immediate deaths and overly apparent disease. Utilizing stealth agents with long incubation periods that can evade detection and disable the immune system were sought after in the Cold War, agents that were geared toward long-term attacks, so that by the time it is realized that such an agent is doing harm, it is often of such a late stage that is hard to correct or contain.

This is why the agents that cause slow chronic diseases became the most successful biological weapons during the Cold War, which is the focus of my first book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. In addition to that, all the better if they could find ways to introduce such viruses into the very medical technologies meant to prevent disease – the vaccine.

While contamination has plagued vaccine manufacturing as an inherent problem in the technology from its inception, the idea of deliberately tainting vaccines is not new in biowarfare history. In fact, even as far back as the Civil War the Confederates accused the North of deliberately tainting their smallpox vaccines with vaccino-syphilis.1 Sabotage of vaccines with specific agents was certainly known in potential and a very sensitive topic in the biological warfare race in motion since the start of the United States of America.2 By the time of the Cold War, the biological warfare race was in full swing and stealth agents were already being developed.

Erich Traub was the godfather of these stealth bioweapons – bioweapons that target the immune system, because it was Traub who discovered the mechanics of how they work when he discovered immune tolerance with LCM Virus beginning in 1935 at the Rockefeller Institute.3 Immune tolerance is chronic immunodeficiency, a paralyzed immune system.

These kinds of stealth agents were being unleashed on America and certainly vaccine contaminants would have been a highly esteemed method of infecting a population with stealth viruses that could cause chronic disease, mental illnesses, and cancers to explode in the decades to follow, which is exactly what we’ve seen, and its continued climbing ever since.

A 2003 declassified CIA assessment titled The Darker Bioweapons Future discusses the mechanisms of stealth viruses as biological weapons and talks about how an enemy could seed a population with a stealth virus that would remain dormant and be triggered later, as binary bioweapons that are effective through two components. It states:

According to the scientists convened, other classes of unconventional pathogens that may arise over the next decade and beyond include binary BW agents that only become effective when two components are combined (a particularly insidious example would be a mild pathogen that when combined with its antidote becomes virulent); “designer” BW agents created to be antibiotic resistant or to evade an immune response; weaponized gene therapy vectors that effect permanent change in the victim’s genetic makeup; or a “stealth” virus, which could lie dormant inside the victim for an extended period before being triggered. For example, one panelist cited the possibility of a stealth virus attack that could cripple a large portion of people in their forties with severe arthritis, concealing its hostile origin and leaving a country with massive health and economic problems.4

This is a striking example of how hidden viruses in vaccines can be turned into biological weapons agents, especially when it comes to the idea of binary bioweapons, where a population is seeded with stealth viruses, like SV40 and additional contaminant viruses of all kinds. The virus lies dormant in hosts for long periods of time, even passing down generations, before being activated by vaccines taken later on, especially by those that containing Pam-3-Cys-like lipopeptides since it will cause serious immunosuppression and immune tolerance, at which point these dormant viruses reawaken and cause serious chronic disease, neurodegenerative disease, and cancers. It is not hard to see how this would be a useful channel for bioterrorism.

All one would have to do is to introduce these stealth viruses into the supply of animals to be used in the manufacture of vaccines, so in the case of polio vaccines grown on monkey kidney cultures, for example, you infect the monkeys where they are sourced in the wild for use, such as the jungles of Africa or Asia. For cell cultures made from animals that are more domesticated, like dogs or hamsters, the process is even easier. Likewise, sera (blood) from horses and other animals is often involved in preparing cell cultures used for growing the vaccine virus, so there are many targets that could potentially enable this contamination to occur and deposit stealth viruses of all kinds into commercial vaccines.

It certainly invites new scrutiny to some of the mass contamination events in vaccine history, most notorious among them is the SV40 problem known to the polio vaccines, where an estimated 200 million Americans (about half the U.S. Population at the time) were exposed to this virus in the uptake of polio vaccines during the 1950s.

Even after the discovery of this virus and the attempt at its containment, batches continued to be tainted, other vaccines also became tainted, and it became a problem that continued plaguing the pharmaceutical industry. Additional strains of SV40 that were not detectable by more modern testing were found in these vaccines, as noted in a 1999 paper, Unique Strains of SV40 in Commercial Poliovaccines from 1955 Not Readily Identifiable with Current Testing for SV40 Infection.

Of course, this could easily be written off as accidental, many contaminates are, but there are some aspects of the polio vaccine development and the people associated with them that are extremely suspicious and the circumstances very alarming, most notably as it relates to a Soviet bioweaponeer named M. P. Chumakov and his friendly American scientists Albert Sabin and Jonas Salk.

But it goes further, because the SV40 saga continues today in the COVID-19 vaccines, with M. P. Chumakov’s son Konstantin Chumakov, having approved the COVID-19 vaccine. The mRNA COVID-19 vaccines used segments from the SV40 virus, and is now showing signs of serious harm, including cancer, bringing the story full circle since the days of his father’s work on the oral polio vaccine.

In the last chapter of my book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I had discussed the polio vaccines and the collaboration between Albert B. Sabin and M. P. Chumakov, and I also took a closer look at Jonas Salk, because of biological warfare activity occurring between the Soviet Union and the United States, it was highly troubling that the FBI would clear Jonas Salk to advise the U. S. Government and manufacture a polio vaccine when he couldn’t pass a background check and was found to have been an active member in many communist front groups. Somehow, despite all this, a second FBI investigation was initiated, probably by compromised FBI agents, and they cleared him despite all the red flags, just as they did for Erich Traub in Operation Paperclip.

It was yet another shock to see the FBI then clear Albert B. Sabin to team up with the Soviet bioweaponeer M. P. Chumakov, traveling back and forth between America and the Soviet Union to collaborate on a polio vaccine that would be given to many millions of Americans at a time when biowarfare activity between these countries was very active. M. P. Chumakov was very active in developing and testing biological weapons in the 1930s with ticks and other insects, which they tested on the restive Muslim and Mongolian populations in Siberia. Chumakov then traveled to East Germany to Insel Riems where Erich Traub was running the most advanced bioweapons program on the planet during World War II. Chumakov met with Traub to gather information on immune tolerance and LCM virus – the model for stealth viruses that – when reactivated – inflict slow, wasting diseases and cancers.

It turns out that Erich Traub’s role in war crimes in World War II made him subject to Soviet blackmail during his time under Russian occupation, and of course the British were also helping to assist him and other Nazis with similar circumstances, to come to America where they would begin a largescale bioterrorism campaign against the United States. Let us also remember that the Soviet Union is more or less a creation of British Intelligence and I talked about how the British were waging biowarfare against the United States since its formation. Britain being no stranger to divide and conquer and playing sides to the middle, their initial bioterrorism campaign on America continued through their go-between – the Soviet Union.

After all the suspect moves on behalf of the FBI clearing people with shady backgrounds and allowing collaboration with Soviet bioweaponeers, we ended up with two polio vaccines, the first one was the inactivated polio vaccine, and the second was the oral polio vaccine (OPV) that M. P. Chumakov developed with Albert Sabin. Both vaccines were contaminated by SV40 – a stealth oncogenic virus that acted very much like Traub’s LCM Virus and would cause very similar neurological diseases and cancers. The fact that Chumakov was meeting with Traub in the years before he and Sabin teamed up is very suspicious. Also, Chumakov’s institute even had expeditions in Africa and Asia at the time which were all KGB intelligence people and could have very easily infected the monkey supply used for vaccine production with similar stealth viruses of all kinds, including SV40.

Additional contamination events with Marburg Virus occurred about a decade after the collaboration with Albert Sabin – the Marburg Virus outbreak of 1967 at the Behringwerke laboratory in Marburg, Germany and another lab in Yugoslavia. This was the older sibling of the Ebola virus that would show up later in Africa, both were severe forms of hemorrhagic fever viruses. Shortly before the outbreak occurred, Chumakov was studying hemorrhagic fever viruses in monkey tissues and in different kinds of cells.

These Ebola-like hemorrhagic fever viruses do not originate in Africa, but actually have their origins in Russian territories like Siberia and the Crimea, such as the Crimean Hemorrhagic Fever Virus, before they ever show up in Africa, but soon it began to show up in the regions surrounding the Congo, and it earned itself the name Crimean-Congo Hemorrhagic Fever Virus. Moreover, just 2 years after Chumakov’s institute had setup expeditions in Nigeria to study arboviruses from monkeys of that area, a new hemorrhagic fever announces itself in the region, Lassa Fever Virus.

They began testing these newly developed agents in the late 1930s, then took them to Africa to continue these testing phases. Africa then unfortunately was turned into a biological weapons testing ground. Certainly, the U. S. has equally taken part in this detestable practice on the unwitting African continent.

When the Marburg Virus outbreak occurred in the labs of Germany (Behringwerke Ag) and in Yugoslavia, they were in the process of manufacturing oral polio vaccines. The virus had been silently infecting the monkeys, in other words, stealth infections that spread to the lab workers and started the dangerous outbreak where people lost their lives and many others were infected and became dangerously ill but survived. The virus had a 30% fatality rate. And this is the reason that stealth viruses would be far more suitable, because then they are more likely to reach the targets of vaccine recipients without starting noticeable outbreaks that alert public health.

The Behringwerke lab was in West Germany, which was under the control of Britain and the United States. Some of the press in East Germany began circulating the idea that the outbreak was the result of the British and Americans running a secret biological weapons program. As a result, they provided M. P. Chumakov with strains of the virus and they never heard another word about it again.

A former KGB officer Alexander Kouzminov talked about plans for such a vaccine sabotage program in his memoir Biological Espionage: Special Operations of the Soviet and Russian Foreign Intelligence Services in the West with one particular memorandum he describes having seen:

In the memorandum one continually met the phrases “The Instance,” “Day X,” and “direct actions.” By “The Instance” was meant the Politburo of the Central Committee of the Communist Party of the Soviet Union. After disintegration of the Soviet Union, “The Instance” came to mean the “President of Russia and his Presidential Council,” The formula “Day X” meant the beginning of a large-scale war against the West. “Direct actions” implied acts of biological sabotage and terrorism against the civilians, the army, and the economy of a potential enemy. “The potential strike targets” meant civil targets, including public drinking-water supplies, food stores, and processing plants; water-purification systems, vaccine, drug, and toxin repositories; and pharmaceutical and biotechnological plants.5

All of the aforementioned information would lead us to conclude that a vaccine bioterrorism program to infect the population with stealth viruses through vaccines was a very realistic possibility, and there are all sorts of unwanted animal viruses in the vaccines that sneak through the detection process and activate later, especially after additional vaccines. So even if many of the contaminants were accidental, some like the SV40 could have been deliberate, based on the shady circumstances surrounding the polio vaccines.

Furthermore, why was Jonas Salk writing books about overpopulation and making alarming statements about how we need to stop medical and scientific advances that keep life going for people because of overpopulation:

A major threat to the species is attributed to the increasing size of the human population, which, in turn, is ascribed to successes in science and technology. This “explanation” has evoked an attack upon science and the exploitation of its technology, to the development of which are attributed many adverse effect upon the human species and upon other forms of life. “Polluters” who befoul the planet affect the “quality of life” and are regarded as a threat to the present and future equilibrium of the species and of the planet. Those who consider themselves on the side of Nature, and therefore of the human species, see others in opposition to both Nature and Man. Hence we are to be concerned not only with Man’s relationship to Nature but with Man’s relationship to himself.6

And why was Jonas Salk saying that we could use viruses to degenerate and test the gene pool of humanity in a way that would cause permanent harm and degeneration to occur, when the SV40 virus that contaminated his vaccine does exactly that? If you think I’m making this up, I’ll pull another quote from his book Survival of the Wisest:

Biologists have discovered many ways in Nature of acquiring such information and of producing new combinations. For example, sexual reproduction, which results in new mixtures of inheritable information, may be seen as a producer of “mutations” in the sense implied above. “Mutations,” as here defined, would also be produced by the introduction, either naturally or experimentally, of a virus into a sperm or egg cell, the genetic information of which would then be incorporated in either the DNA or the RNA and transmitted. Such new information might be advantageous or disadvantageous. Nevertheless, it would be transmitted hereditarily, having become part of the organism, whose survival value would then be tested in the process of natural selection. Other ways of altering inheritable information are by the application of X-rays to germinal tissue, or by chemical means; these effects are mediated by DNA or RNA alterations. Purely accidental errors, or copying errors, in the course of gene replication of protein synthesis, produce similar effects. In all instances the survival value of the products for continued evolution are determined subsequently.

Similarly, in the metabiological realm, new perceptions arise from time to time, which occur spontaneously, or by deliberate search. These have effects analogous in a way to new inheritable biological information in its transmissibility from generation to generation by cultural means. New perceptions can also be spread, as would the hypothetical virus proposed above, to alter, favorably or unfavorably, the behavior of the individual arising in this way, those related to him, as well as those to follow. In the metabiological realm revolutionary ideas may be seen as part of the process of evolution, equivalent to the occurrence of “mutations” in the biological domain; they are then subjected to the process of “selection for survival” to be retained until changed or eliminated.7

The SV40 problem has not gone away, it is simply being ignored, the public health system does not even test for it, they aren’t doing anything to address the biggest mass infection event with stealth cancer viruses that infected over 200 million Americans during the polio vaccination program, even though they did have a congressional hearing in the early 2000s, PREVENTING ANOTHER SV40 TRAGEDY: ARE TODAY’S VACCINE SAFETY PROTOCOLS EFFECTIVE? As usual with congressional hearings, they go nowhere and no one is held accountable. However, it didn’t end with SV40, because many more adventitious contaminant viruses have been showing up in every other vaccine. It is a problem that they refuse to adequately study and address.

In the 1970s, U. S. Public Health officials were concerned with nationwide outbreaks of LCM Virus that were infecting hamsters across the country. On April 14, 1974, The New York Times published “Hamsters Killed to Prevent the Spread of Mild Meningitis,” indicating that authorities were involved in a nationwide culling of hamster lots infected with LCM Virus, and this is alarming especially since hamsters were being used as a source for growing vaccine viruses in baby hamster kidney (BHK) cell lines. Multiple journals reported outbreaks of LCM Virus among scientists and medical personnel at the time, and they found that cell lines used in research were sources of the outbreak. For how long these hamsters were infected is not known. LCM Virus is a virus known for its ability to disable the immune system and bring on immune tolerance, as it was the virus Erich Traub discovered immune tolerance with.

Epstein-Barr Virus, or EBV, is another virus that is commonly found in the population that turned up in Africa in the late 1950s causing cancer in the African population and was later found to be infecting the entire United States, and very likely come in from vaccines. Many of the other common herpesviruses seem to be of the same source, and all of the 8 human herpesviruses cause a bewildering number of disease manifestations and cancers. These are issues that need to be looked at with much more scrutiny and attention.

Certainly, some of the contamination events are accidental, but when you look at the SV40 situation as a whole and the shady collaborations and suspicious activities between Sabin, Salk, and M. P. Chumakov, the interest in SV40 and other stealth viruses that caused immune tolerance, like Erich Traub’s LCM Virus, and knowing that M. P. Chumakov’s son was running Vaccine Safety and Review at the FDA and approved the COVID-19 vaccine, which used material from SV40, and is now showing signs of serious harm in the population, there are certainly a lot of coincidences to be considered, which lead us to consider more deliberate, sinister possibilities.

For more of this story, pick up a copy of my book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare and you will embark on a journey to understand the esoteric art of stealth biological warfare and the science of immune tolerance that explains much about the chronic disease, mental illness, and cancer crises rocking the United States

This book details out the esoteric history of biological warfare in a way that no other book has done, based on only official records, documents, science and medical journals, former intelligence officers, and more. The history of this war goes much deeper than any other book on the subject has presented, based on understandings and studies of science that have been purposefully buried and obscured. The author collected and studied the work of one of history’s most exceptional yet infamous pioneers in virology and immunology, a German scientist by the name of Dr. Erich Traub, for several years, in the process of writing this book, a process which perhaps no one else has managed to undertake, until now.

I would like to present to you my new Substack publication for the Biosecurity Ethics and Immune Tolerance Awareness Initiative. The Biosecurity Ethics & Immune Tolerance Awareness Initiative exists to educating the public about the role of immune tolerance in chronic diseases, neurological and neuropsychiatric disorders, and cancers. We further educate and advocate for ethical biosecurity practices and informed policy decisions made in full transparency, through ethical guidelines, working to close critical vulnerabilities, and defend actual national security from foreign influence in public health and biodefense strategies, rather than using National Security as guise to hide scandals and evade accountability.

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Biosecurity Ethics & Immune Tolerance Awareness Initiative

The Biosecurity Ethics & Immune Tolerance Awareness Initiative

Welcome to the Substack of the Biosecurity Ethics and Immune Tolerance Awareness Initiative. The Biosecurity Ethics & Immune Tolerance Awareness Initiative exists to educating the public about the role of immune tolerance in chronic diseases, neurological and neuropsychiatric disorders, and cancers. We further educate and advocate for ethical biosecurit…

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2 years ago · A. W. Finnegan

The Truth of Chronic Disease in America Shall be Unveiled. The Health of All Depends on it.

In 1960, the science of slow, chronic disease and persistent infections, once baptized “immune tolerance” was obscured and marginalized to the realm of organ transplantation and its recipients, as the 1960 Nobel Prize was given in error to Frances MacFarland Burnet and Peter Medawar for transplantation even though the two never worked together nor were they nominated together by anyone. However, it was Erich Traub, who had discovered it in 1935 while with Lymphocytic Choriomeningitis Virus (LCM), and correlated to a similar effect coined “immune paralysis” after injection of large doses of pneumococcal polysaccharide antigens. However, the Nobel Prize “given in error” appears more likely to have been a deliberate choice as it would have devastated Western immunology and the science of infectious disease determined by antibodies and observable inflammation. Equally so, it would have flipped vaccine science on its head and exposed the true nature of vaccine-induced “immunity” as a slow destruction of the immune system rather than building it up as strong and healthy.

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Erich Traub first elucidated the condition during vaccine research at the Rockefeller Institute in 1935 when he injected the brains of mice with foreign proteins, reactivating dormant LCM virus from within the mice, causing an epidemic from scratch. The result was a slow chronic disease via immunosuppression and persistent viral infection that could be passed congenitally from mother to newborn, maintaining itself through generations, while silently degenerating the genetic integrity of subsequent generations, plaguing them with chronic disease, neurological syndromes/wasting disease, and cancer.

In short, antigenic stimuli were behind this condition which produced chronic immunodeficiency and reactivated dormant viruses from within the body, invited additional opportunistic infections to create a highly complex and complicated chronic disease accompanied by neurological/neuropsychiatric disorders, wasting disease, and cancer. It would present in the absence of detectable antibodies and little to no outward inflammation. Likewise, Traub’s experiments demonstrate how a vaccine antigen too toxic for the body can cause new outbreaks with other diseases already dormant in the vaccine recipient.

Since the 1960s when the infectious origins of immune tolerance were buried and obscured, the science of chronic disease and neurological/neuropsychiatric disorders began working in reverse. Public Health has been ignoring the underlying condition at the root of these diseases for decades by using tests and diagnostics that evade the evidence of the condition by using the wrong biomarkers of disease and calling it “evidence-based medicine.” This so-called Evidence-based medicine only uses antibody response and inflammation as its criteria for diagnosis but immune tolerance is the polar opposite. There are ways to detect and diagnose it using other biomarkers, but they use different biomarkers than that used to study acute diseases marked by robust antibody response and heavy inflammation. This then allows them to write off the condition as non-existent and psychosomatic in nature when in fact it is anything but a disease of the imagination.

This sleight of hand used by American public health as its gold standard for diagnosis has left millions of Americans out in the cold, sick and demoralized with doctors illegitimizing their health complaints as psychosomatic, yet the science is all there demonstrating the precise scientific mechanisms of these complicated health presentations, stealth infections that destroy slowly, in the absence of antibodies and inflammation, all the while allowing for the pharmaceutical firms to evade accountability when the same complex condition caused by vaccine antigen brings on these complicated and often incurable diseases and adverse events. Nowhere is this more apparent than the recent wave of sick people injured by the COVID-19 vaccine.

1. The Time is Now - the Unveiling Begins…

The acknowledgement of Immune Tolerance and the chronic spectrum of disease due to the effect of an antigen’s ability to exhaust and burn out the immune system, if acknowledged, would flip vaccine science on its head, along with the diagnostic standard that tells us inflammation is the cause of all disease, when in fact there is an entire spectrum of disease that presents in the absence of inflammation with little to no antibody response.

Understanding these mechanisms would expose the underlying nature of all vaccine injuries as the result of inhibitory effects on the immune system and would show that compulsory vaccination is not by any means a healthy, invigorating process. It would demonstrate that vaccines are tolerizing and exhausting the immune system rather than giving true immunity and often at great cost to the overall health of the vaccine recipient, bringing chronic diseases and secondary neurotropic effects to the brain and central nervous system to plague them for many years to come.

If this had been addressed for what it was, the entire science and industry of vaccination, diagnostic testing, and healthcare in America would be forced to face the music about the harm they have been doing for decades through the deliberate omission of Traub’s findings. This has resulted in and will continue to destroy the health and well-being of our species the longer it goes unaddressed. The sheer volume of vaccines in today’s immunization schedule guarantees doom for these children by the time they reach adulthood if not sooner.

2. Rebuild the Health & Well-Being of America by First Properly Identifying the Underlying Nature of Chronic Disease - Immunosuppression.

The science of chronic disease as immune tolerance via chronic immunosuppression has been there all along. Studies already exist and show definitively that not only does it include the explosion of chronic disease, but that neurological/neuropsychiatric disorders, and cancers, can all be directly linked to these mechanisms. There is no need to start from scratch with studies reaching in the dark to figure out what is going on, there is already voluminous amounts of published research that establishes the nature of chronic disease, mental illness, and cancer due to the immunological paralysis that has been coined “immune tolerance.” In short, Immune tolerance is immune paralysis.

Erich Traub had spent his entire career studying the phenomenon and plenty of the biodefense circles had been following up on his findings for decades to come. It has already been established that lipoproteins or antigens alone are able to elucidate this condition in complete stealth due to the immunosuppressive effects on the immune system. This can happen following vaccinations of all kinds, as well as from unethical biodefense practices using what have been touted as harmless simulants used in open-air tests since the 1950s. Lyme disease had been one such simulant spread through ticks on shorebirds in the early 1950s under the supervision of Erich Traub on Plum Island, using strains of Borrelia anserina that he had acquired from Rockefeller-funded psychiatrist Franz Jahnel through his student Werner Schäfer in 1939.

3. Public Health Officials Cannot Play Dumb and Feign Ignorance. They Have Known About Tolerance for Decades and Records Prove it.

While Erich Traub discovered and pioneered the science of immune tolerance and persistent viral infections, the scientific community and later public health officials in the United States have known about the infectious origins of “immune tolerance” for decades, and in 1971, scientific conferences like “Immunological Tolerance to Microbial Antigen” held in New York was attended by scores of prominent American scientists and vaccine developers like Maurice Hilleman, Merrill W. Chase, Robert J. Huebner, John Hotchin, Ludwik Gross, and more. In fact, they invited Erich Traub to the conference but regrettably he could not attend, and they paid Erich Traub homage for being the discoverer of infectious immune tolerance following his early work on the condition with the virus of Lymphocytic Choriomeningitis Virus (LCM) from 1935 onward. John Hotchin then dedicated his 1971 Virology Monograph Persistent and Slow Virus Infections with the opening page “To Eric Traub who started the whole thing.”

Furthermore, many leading American public health officials like Erich Traub’s Rockefeller colleague Albert B. Sabin, or Sabin’s rival - the inventor of the inactivated polio vaccine (IPV) - Jonas Salk, was also very much aware of it, as noted in his overpopulation monograph Survival of the Wisest. The same could be said for Konstantin Chumakov, who was leading Vaccine Safety and Review at the FDA in 2021 when he approved the COVID-19 vaccine to be rolled out. He got into the American public health system by Sabin’s vouching for him. Anthony Fauci’s early career shows he would have been well-versed in how immune tolerance works. Evidence suggests not only did they understand the nature of immune tolerance, they were deliberately using it as a defense strategy, while misleading the public to believe something very different than the truth. In 2012, The Bill & Melinda Gates Foundation funded research “Disease Tolerance as a Defense Strategy” proving they knew full well what they were doing with vaccine countermeasures.

Using immune tolerance as a defense strategy is a terrible idea considering that when it is induced, any suppressing of severe disease is followed by an avalanche of complex chronic diseases, neurological/neuropsychiatric disorders, and cancers! They had all the scientific research findings to demonstrate this and fully understand it, yet they decided to use it as an acceptable form of “immunity” while being completely dishonest to the public about what was really being done. Even more alarming, they knew that the modern medical diagnostic testing and treatments available today would fully evade recognition of the cascade of health problems that would follow! This is because the “evidence-based medicine” used as today’s gold standard for medical diagnosis is not designed to identify the condition at the root of the long and complex road of disease that follows. These are crimes against humanity when one truly understands how far-reaching the harm goes and the level of deceit used to unleash it!

4. Join Us in Taking Back Health and Unveiling the Truth about Immune Tolerance, it is Not an Acceptable “Immunity.”

This Substack will be the foundation for educational material that will be used to put together what I hope will eventually become a non-profit organization to begin actively working to change the landscape of public health and biodefense, or at least to give the sick Americans an answer of validation for a very real disease despite the public health’s insistence that they are imagining things. It has gone on for far too long, the lies need to end and the nature of this condition and its history must now be unveiled…

5. RFK Jr’s Upcoming Health Initiative Will FAIL if the Origins of Immune Tolerance via Toxic Antigen is Not Understood or Addressed.

It is commendable that RFK Jr. is stepping up to the plate to demand an end to the chronic disease explosion in America. However, if the root causes are not addressed and the factors that cause these diseases are left untouched and able to continue, then his mission will be a dismal failure and will make this situation even worse. We cannot simply point the finger at metals in vaccines as the cause of autism because it is not the metals but the main ingredients themselves, the antigens, which trigger the immunosuppression and resulting virus reactivation, which ultimately delivers the neurotropic effects to the brain that cause autism, neurological disorders, neuropsychiatric disorders, ADD/ADHD, and beyond.

Furthermore, these certain antigens responsible for immune tolerance are also potent mitogens, which cause mitosis, and it is in the mitotic processes which bring forth cancer through the upregulation of telomerase. Cancer can be brought on from the reactivation of latent virus, many of which in the herpesvirus family, are oncogenic when reactivated from latency, not to mention, neurotropic. It cannot be avoided that the vaccines have to be dealt with because they are inducing systemic immune tolerance en masse. We could find safer more innovative ways to combat disease if we provided the right atmosphere and allowed scientific researchers to work creatively and through innovation rather than enslavement by those funding the research to only research what they deem acceptable.

6. The Dark Triad of Immune Tolerance: An Occam’s Razor that Links Chronic Disease, Neurological/Neuropsychiatric Disorders, and Cancers to One Condition

Simply put, immune tolerance induced by antigen brings on what I have termed The Dark Triad of Immune Tolerance. A diabolic triplet of disease manifestations that cascade upon its victims when the immune system is suppressed by infectious mechanisms and antigen. Here below is a diagram I have designed to illustrate how a certain class of antigens found on numerous pathogens and viruses are able to paralyze the immune system and bring on a triplet of chronic disease, neurological/neuropsychiatric disorders, and cancers!

However, because of the nature of destabilizing the immune system, this triplet will present in infinite variation, so that no two unravel in the same exact way. Because of the way our public health system and medicine likes to diagnose diseases and disorders under very specific definitions classed as specific disease entities and disorders, this obliterates all distinctions separating them and causes them all to overlap and seep into one another like a melting pot for all classes and definitions of disease.

Immune Tolerance has been hiding in plain site all along, but desperately needed someone to come along, connect all the dots and teach us the extensive history of immune tolerance, its inherent connection to the work of Erich Traub and the biological weapons race, as well as devastating the paradigms of Western immunology and vaccine science. It has gone by many names, including but not limited to - immune paralysis, endotoxin tolerance, post-polio syndrome, post-influenza fatigue, post-viral syndrome, post-viral fatigue, post-infection syndrome, post-treatment Lyme disease syndrome, post-rickettsial syndrome, post-sepsis syndrome, post-vaccinal syndrome, post-vaccinal encephalitis, post-malaria neurological syndrome, myalgic encephalomyelitis/chronic fatigue Syndrome (ME/CFS), Gulf War Syndrome (GWS), and of course the newest addition: long-COVID.

7. The Sleeper Agent: A Preliminary Introduction to the History of Immune Tolerance and its Pioneer, Dr. Erich Traub, to Manufacture Stealth Biological Weapons

My first book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare (Trine Day 2024), details the entire history, discovery, and usage of immune tolerance in the biological weapons race, serving to tire, exhaust, and overwhelm the enemy instead of causing immediate fatal disease. These strategic weapons were far more effective through a long-term strategy in destabilizing nations like the United States of America, and by the time it starts to become really apparent, most of the damage is already done by the Dark Triad of immune tolerance and virus reactivation.

This book will not only provide a preliminary course on the science and discovery of immune tolerance, but it will provide a detailed history lesson on the context in which it was buried and obscured. It will educate you with an in-depth course through the complex labyrinth of the biological weapons race, It will initiate the reader into the concealed nature of its study and development, the complex wars of intelligence, espionage, and biological sabotage used to wage it. It was from within this atmosphere that immune tolerance emerged. Its place in medicine and healthcare was quickly silenced and this leaves us with some very disturbing possibilities on the nature of hostile foreign influence quietly shaping American public health policy and biodefense activities to work against us.

It is astounding to me just how inaccurate some of these so-called “fact-checked” articles can be when they write articles claiming to give the “facts” and stand as the arbiter of truth. These writers sometimes know next to nothing about the subject they write about, which is clear to those that do know about it. They jump to erroneous conclusions citing studies that are totally inconclusive and making unscientific claims and the fact checkers repeat it as though it is scientific fact, Lyme disease is one example.  

Recently, I came across an article “fact-checked” from April 2022 “Fact Check: Lyme Disease Was NOT Invented In A Lab In 1975 -- Its Bacteria Is Thousands of Years Old,” [1] by: Marlo Lee writing for Lead Stories, a “fact checking” site that is stamped with approval by Meta (Facebook) and the International Fact-Checking Network (IFCN). The article was about Lyme disease originating from the Plum Island laboratory in 1975, due to Erich Traub’s work there.  

What I agree with in this article, is that Lyme disease was not invented at the Plum Island lab in 1975, it was weaponized long before, in Germany, but Traub conducted tests there with his weaponized strains, but let’s be clear about what we mean by weaponized. The actual spirochete, before it was weaponized, has been around for perhaps millions or billions of years, it was a bird strain of Borrelia called Borrelia anserina,[2] and it is true that it did not originate from Plum Island in 1975, because it had been weaponized in Germany starting in 1939, and it had several developments, but may have been weaponized once more during Traub’s return to the United States after WWII and conducted tests with it on Plum Island.  

However, being weaponized does not mean it was created from scratch, it weaponized the naturally existing Borrelia anserina with naturally existing viruses and lipoproteins so that when complete, it was different from the earlier Borrelia anserina. It had new properties and could infect many new species of animals and humans, due to the methods Erich Traub used in bioengineering, animal passages, and this method has been explained in other articles.  

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The article cites an article from 2004 from The New York Times about Michael Christopher Carroll's book Lab 257: The Disturbing Story of the Governments Secret Plum Island Germ Laboratory, to show that a spokeswoman from the Agricultural Research Service (ARS) of the USDA voices no association she knows that Erich Traub had to Plum Island.[2] However, this is wrong, and the ARS official probably knew it was wrong and was saying it out of damage control.

My book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, shows that Traub was employed by the Agricultural Research Service at Plum Island and he was brought there because of the original public law for its construction, Public Law 496, 80th Congress,[3] as a chief scientist for the Agricultural Research Service at the Greenport, Long Island station of the ARS, which is Plum Island, and FBI documents actually confirm this, [4] but fact-checkers haven’t looked at any of these documents. They only bolster the official talking points coming from “authorities” but they don’t actually specialize with expertise about what they write. 

Next, the idea that Lyme disease is thousands of years old is totally unsubstantiated and an unscientific claim. She says in the article, “Scientists in Italy found a 5,300-year-old mummy who had the oldest known case of Lyme disease, according to genetic tests performed after its discovery.” No, the scientists did not find Borrelia burgdorferi, or even Borellia afzelii, nor Borrelia garinii, three species of Borrelia responsible for Lyme disease. They found merely traces of what they thought might be from Borrelia spirochetes, but they said further testing is necessary to confirm it was even Borrelia, but what their published research about it shows us is anything but conclusive: 

While several reads were specific for Borrelia, the 60% coverage still represents an upper boundary as reads may map to other species besides Borrelia. [5]

Furthermore, they failed to point out the incompetence of the Next Generation Sequencing (NGS) technology for Whole Genome Sequencing (WGS), and particularly for Borrelia burgdorferi. It is highlighted in a paper specifically addressing the inadequecy of Whole Genome Sequencing for Borrelia burgdorferi: 

However, the power of NGS has not yet been fully harnessed for vector-borne and zoonotic disease (VBZ) systems, the majority of globally emerging infectious diseases. [...] This is due to the high ratio of host (the arthropod vector or the reservoir host) to pathogen DNA present in mixed DNA samples [11, 12]. The overwhelming presence of this exogenous DNA (which may also include commensal bacteria, endosymbionts, and environmental microbes) renders shotgun sequencing inefficient and cost-prohibitive.

[...]  

The agent of the most prevalent vector-borne disease in the US, the Lyme disease bacterium, Borrelia burgdorferi sensu stricto, exemplifies this common hurdle to genomic study for many VBZ systems. [...] Shotgun approaches for WGS of pathogens directly from field samples are inefficient due to the excess of contaminating host DNA present in the samples, which result in very low sequence coverage of the low copy number bacterial genomes present. [6]

The scientists conducting the sequencing on the mummy failed to disclose this fact when they suggested that Lyme disease was present in the mummy. But it was repeated by Live Science and the fact-checker as though it was an absolute fact that the mummy had Lyme disease.  

The fact-checker then goes on to say, “Researchers at Yale School of Medicine found that Borrelia burgdorferi, the bacterium that causes Lyme disease, existed for at least 60,000 years in the northeastern region of the United States.” Here is another instance of reporting something as a fact that was entirely inconclusive and based on a mere guess. The Yale researchers made this conclusion off a totally unsubstantiated theory based on 146 ticks collected from the range of 1984-2013, and by looking at mutation rates of genes and phylogeography. For those who don’t know what that means:  

Phylogeography is the study of the historical processes that may be responsible for the past to present geographic distributions of genealogical lineages. This is accomplished by considering the geographic distribution of individuals in light of genetics, particularly population genetics. 

[...] 

Past events that can be inferred include population expansion, population bottlenecks, vicariance, dispersal, and migration. Recently developed approaches integrating coalescent theory or the genealogical history of alleles and distributional information can more accurately address the relative roles of these different historical forces in shaping current patterns. [7]

Just to be clear, when something is inferred, it means that it is to “form an opinion or guess that something is true because of the information that you have.” Furthermore, this theory is made without taking into consideration the factors that interfere with this theory, like man-made intervention such as bioengineering.  

Moreover, it is further hampered by limitations to their study, which I would describe as entirely unreliable, due to the fact that they cannot get an accurate picture of each specific sample of Borrelia burgdorferi genes since it is often picking up multiple infections in one sample, and the incompetence is further laid bare:  

One limitation to this study is that phylogenies are inferred from consensus bacterial sequences from each individual tick sample. [...] However, the consensus sequence may alternatively represent a chimeric sequence, a combination of segments of the multiple co-infecting haplotypes. With short-read sequence data used here, we are unable to reconstruct multiple bacterial haplotypes within a single sample. Longer-read sequencing will enable sequencing multiple bacterial genomes from individual tick vectors in the future. [8]

Now, essentially, this means that they cannot accurately read each sample, and at best it is a guess, and keep in mind, the data gathered from each guessed sample are then interpreted as a whole to make yet another guess about its possible evolution through phylogeography. 

Next, the Yale researchers also cite a paper claiming that Lyme disease was found in 2 mouse tissue samples from 1896, [9] but that paper was refuted by Richard Marconi et al., from the NIH Rocky Mountains Laboratory, after pointing out that the set of primers they used for testing were not reliable. [10] In these two mouse tissue samples, they only found tiny fractions of the outer surface protein OspA plasmid which contain material shared with viruses of the poxvirus family. It is also extracellular DNA which changes all the time and assimilates DNA from foreign sources,[11][12] making it totally unscientific to say that it is evidence of a Borrelia burgdorferi infection, and they specifically address this in one of their other papers, explaining that they can find “plasmid DNA (which contains telomeres that are homologous to those of vaccinia virus) in human tissues independent of B. burgdorferi infection.” [13] 

I rest my case. I hope this points out for the reader just how the “authority” talking points cannot be trusted regarding this matter, and for pretty much any other. One always has to investigate for oneself. They have been actively trying to cover-up these misdeeds for decades and they were using the scientific community to do it, just as they did with the Lyme Disease diagnostic testing, which the organization TruthCures has so eloquently shown. My book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare tells the story of Lyme disease and biological warfare, for the first time, and is able to link it to the work of Dr. Erich Traub in Germany starting in 1939 and it had several developments during World War II and it was further weaponized upon his return to American shores to work for the military and USDA through Operation Paperclip.  

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Endnotes

[1] Lee, M. (2023, May 15). Fact check: Lyme disease was not invented in a lab in 1975 -- its bacteria is thousands of years old. Lead Stories. https://leadstories.com/hoax-alert/2022/04/fact-check-lyme-disease-was-not-invented-in-a-lab-in-1975.html

[2] Walker, R L et al. “Shared flagellar epitopes of Borrelia burgdorferi and Borrelia anserina.” Veterinary microbiology vol. 19,4 (1989): 361-71. doi:10.1016/0378-1135(89)90101-6

[3] Congressional Hearing. (1970, January 1). Legislative history, public law 496 - 80th Congress, Chapter 229 - 2D session, S. 2038 : United States, Department of Agriculture, office of the general counsel : Free download, borrow, and streaming. Internet Archive. https://archive.org/details/PL80496/page/n23/mode/2up

[3] Rather, J. (2004, February 15). Heaping more dirt on Plum I. (published 2004). The New York Times. http://www.nytimes.com/2004/02/15/nyregion/heaping-more-dirt-on-plum-i.html 

[4] National Archives. RG 65 Erich Traub, (Declassified FBI Investigations on the Loyalties of Erich Traub). Federal Bureau of Investigation (FBI): NARA., Doc. # QO1-458431291

[5] Keller, A. et al. New insights into the Tyrolean Iceman’s origin and phenotype as inferred by whole-genome sequencing. Nat. Commun. 3:698 doi: 10.1038/ncomms1701 (2012). 

[6] Carpi, G., Walter, K. S., Bent, S. J., Hoen, A. G., Diuk-Wasser, M., & Caccone, A. (2015). Whole genome capture of vector-borne pathogens from mixed DNA samples: a case study of Borrelia burgdorferi. BMC Genomics, 16(1). doi:10.1186/s12864-015-1634-x

[7] Wikipedia. (2024b, March 12). Phylogeography. Retreived from: https://en.wikipedia.org/wiki/Phylogeography

[8] Walter, Katharine S et al. “Genomic insights into the ancient spread of Lyme disease across North America.” Nature ecology & evolution vol. 1,10 (2017): 1569-1576. doi:10.1038/s41559-017-0282-8

[9] Walter, Katharine S et al. “Genomic insights into the ancient spread of Lyme disease across North America.” Nature ecology & evolution vol. 1,10 (2017): 1569-1576. doi:10.1038/s41559-017-0282-8

[10] Marconi, R T et al. “Variability of osp genes and gene products among species of Lyme disease spirochetes.” Infection and immunity vol. 61,6 (1993): 2611-7. doi:10.1128/iai.61.6.2611-2617.1993 

[11] Marconi, R T et al. “Variability of osp genes and gene products among species of Lyme disease spirochetes.” Infection and immunity vol. 61,6 (1993): 2611-7. doi:10.1128/iai.61.6.2611-2617.1993 

[12] Zumstein G, Fuchs R, Hofmann A, Preac-Mursic V, Soutschek E, Wilske B. Genetic polymorphism of the gene encoding the outer surface protein A (OspA) of Borrelia burgdorferi. Med Microbiol Immunol. 1992;181(2):57-70. doi:10.1007/BF00189424 

[13] Persing, DH et al. (1994). Target Imbalance: Disparity of Borrelia burgdorferi Genetic Material in  Synovial Fluid from Lyme Arthritis Patients. Journal of Infectious Diseases, 169(3), 668–672. doi:10.1093/infdis/169.3.668 

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In my recently published book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I concluded the book examining some of the cozy relationships and collaborations between American scientists and Soviet bioweaponeers like M. P. Chumakov. M. P. Chumakov was discussed at length throughout the book and played a major role in testing out some of the Soviet Union’s bioengineered diseases on the restive Muslim and Mongolian populations in the Siberian regions of the U. S. S. R. in the 1930s.  

They tested tick and insect-borne plagues like tick encephalitis and hemorrhagic fever viruses which would later evolve into the Marburg and Ebola viruses found in Africa much later. M. P. Chumakov even met with Erich Traub at his Insel Riems facility in East Germany several times in 1947 to consult with him about Lymphocytic Choriomeningitis Virus (LCM). This was the model virus that Erich Traub spent his entire life studying to understand stealth infections that destroyed the immune system and brought secondary neurotropic effects and cancers. It is quite a coincidence that Chumakov’s collaboration with Albert B. Sabin and Jonas Salk on polio vaccines were contaminated by a virus that acted in striking parallel to Traub’s LCM virus and infected up to half of the U. S. population through tainted polio vaccines. This virus was called simian virus 40, or SV40.  

Albert B. Sabin, inventor of the oral polio vaccine (OPV), collaborated and developed a cozy friendship with M. P. Chumakov, and Chumakov worked with Sabin on getting the vaccine onto the market. Sabin also befriended Lev Zilber, who led the Siberian expeditions testing these new bioweapons, and he likewise befriended V. M. Zhdanov, a prominent Soviet virologist and bioweaponeer. He also befriended a KGB scientist, Sergei Drozdov, who had penetrated the World Health Organization (WHO) in Geneva. Sabin took trips to the Soviet Union to work with Chumakov and attend virology conferences there and in the USA, in which he would regularly exchange viruses and serums of all kinds with these Soviet “Friends.”  

As this was going on, Chumakov was conducting research on the side, on all kinds of biological warfare agents like Q fever, West-Nile Virus, and the infamous hemorrhagic fever viruses that eventually evolved into Lassa Fever, Marburg Virus, and Ebola Virus. All three viruses cause very similar disease although Marburg and Ebola are very different viruses compared to Crimean Hemorrhagic Fever virus, which earned the name Crimean Congo Hemorrhagic Fever (CCHF) after it was brought to Africa and tested there by Soviet expeditions not unlike those in the Siberian regions in the 1930s, as this virus had its start there after Chumakov tested the virus on the restive Muslim and Mongolian populations with Lev Zilber. 

That Sabin was allowed to team up with these serious names in the biological warfare program of the USSR is almost unfathomable, especially when the Soviet Union was eventually exposed to Western Intelligence having a massive biological weapons program to crush the West.  

What is particularly interesting here is that according to M. P. Chumakov’s son, Konstantin Chumakov, who recently approved the COVID-19 vaccine leading the Vaccine Safety and Review at the FDA, the Soviet Union’s public health officials never had any plans to initiate or test a new vaccine. So, it begs the question, “why was Sabin taking trips to the Soviet Union to work with Chumakov if there were no plans to test it or put a new polio vaccine into circulation there?” Unless, of course, it was being done for another purpose by another authority, like the KGB or Soviet Intelligence. According to Konstantin, in Birth of A Cold War Vaccine:

“Sabin publicly gave credit to my father and the Soviet system whose organization made such large trials possible,” Konstantin says. “But I’m not sure my father ever told Sabin the true story behind it. What actually happened—according to my father— went like this:

“My father couldn’t get permission for a really big clinical trial. A lot of people in the Health Ministry were opposed to it. He was told, basically, ‘We have the Salk vaccine, and it works fine, so there’s no reason for you to test the live virus.’ Well, my father decided to go around them.

“In the Soviet Union there was a higher authority — the Politburo [then known as the Presidium of the Central Committee], which consisted of a small group of Communist Party officials who could overrule everybody. At the time, Anastas Mikoyan was the Politburo member responsible for public health. Mikoyan was not a medical man — he was a political figure who went back to the revolution.

But he and my father were well acquainted. Mikoyan may have appointed him to head the polio initiative in the first place.” Refusing to accept the ministry’s decision not to grant permission for the oral vaccine tests, Chumakov picked up one of the red telephones provided for the exclusive use of the most powerful people in the Kremlin — he was not among them — and dialed Mikoyan’s number.

As Chumakov related the story to his son, he got right to the point and asked Mikoyan’s approval to proceed with the live virus vaccine tests.

“Are you sure this is a good vaccine, Mikhail?” Mikoyan asked. “And that it’s safe?”

“Yes,” the virologist replied. “I’m absolutely sure.”

“Then go ahead,” Mikoyan said.

“That was it,” says the younger Chumakov, whose account rings true with others familiar with the principals. “The only permission he had was verbal, over that Politburo hotline. Of course, the health minister was unhappy, but there was nothing he could do.”

It must be asked, if Chumakov was not among the most powerful people familiar with using the red phones, just how would he have immediately known the proper digits to dial Mikoyan? Sinister motivations are far more likely in light of what we later learned about the Soviet Union’s massive biological war machine. It is interesting to note that Chumakov also worked to some degree with Jonas Salk on his polio vaccine. Both of these were contaminated by the oncogenic SV40 virus, and it is no surprise that cancer is now exploding in the West, much like Erich Traub’s Rockefeller mice after thoroughly infected by the LCM virus causing a massive rise in lymphomatosis. 

In 1967, Marburg virus first appears at the Behringwerke AG labs causing a fatal outbreak among lab workers after they began pressing up monkey kidneys to be used foir making the Sabin-Chumakov oral polio vaccine. The virus was present in the monkeys causing silent infections before erupting in the lab workers who contracted the fatal sibling of Ebola virus, Marburg Virus. In the years leading up to the incident, Chumakov can be seen conducting extensive research on these hemorrhagic fever viruses and his institute had several expeditions down in Africa at the time, like in Nigeria, where Lassa Fever also surfaces for the first time. The monkeys used were said to have been imported from regions around the Congo, where of course the Crimean Hemorrhagic Fever virus also begins to establish itself. In the wake of the Marburg Virus outbreak, the Soviet Union begins to imply that West Germany had been secretly developing biological weapons at the time, and who but M. P. Chumakov is there to receive strains of the virus to determine whether or not it was part of a biological weapons program, but after studying the virus, they said nothing more about it. This was most likely because the virus was actually developed and weaponized by the Soviet Union. Ken Alibek also talked about how they further weaponized Marburg Virus in his book Biohazard.  

In the 1930s, M. P. Chumakov was testing hemorrhagic fevers on mentally ill patients, according to declassified CIA reports, and it establishes the fact that Chumakov knew these infections would be silent in animals, giving a layer of stealth should the Soviet Union consider stealthily infecting the supply of monkeys sourced from the jungles of Africa and abroad to use for tissue cultures in producing vaccines.

What a wonderful collection of coincidences we have here, and even more amazing, that M. P. Chumakov’s son Konstantin Chumakov had been running vaccine safety and review at the FDA for many years and just recently approved the COVID-19 vaccine in 2021, which now has been shown to cause chronic disease and promote cancer growth. Without making any claims or accusations against Konstantin, I am fully justified in having the opinion that after review of all the facts about his father and the details surrounding his rise in Western public health at the behest of Albert Sabin, this position is too sensitive and vulnerable to put someone with his background, being that his father was perhaps the most important of all the bioweaponeers under Joseph Stalin in the Soviet Union. Konstantin said in an interview with Lisa Walker that all of the top scientists at his Moscow University, left the Soviet Union and now fill prominent positions in Western public health and academia:

KC: […] I mean the best testimony that everybody is here now doing extremely well. I mean practically all our graduates are now very highly successful American scientists. Some of them are Department Heads, Lab Chiefs, Full Professors, and it all came, everybody who came from this department are doing extremely well.

LW: What about, I hope that the people who stayed in Russia are doing well, or is that your yardstick is that they’re in the US?

KC: Yeah, because in Russia, there is nobody who stayed. I mean I know a couple of guys who stayed there, but everybody else left. [1]

Vladamir Putin, whose grandfather Spiridon, was Stalin’s personal food taster and chef, still praises and idolizes Joseph Stalin as an effective manager, and it is Konstantin’s brother Petr Chumakov, another spawn of M. P. Chumakov, who advises Putin in Russia’s modern biodefense. The coincidences just keep on coming...  

Read all of this and more in my new book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, now available at Amazon and other book vendors... 

[1] Walker, Lisa. Konstantin Chumakov Interview 2005. NIH History Office, National Institutes of Health (NIH), 25 Apr. 2013, https://history.nih.gov/archives/downloads/konstantinchumakov.pdf Accessed 30 Oct. 2019.

https://www.youtube.com/watch?v=tNO-hogxE4E&t=1033s

Dr. Erich Traub is a mysterious character with a long, rich history and expertise in creating stealth biological weapons that evade tests, confuse diagnosis, and torment the afflicted with slow, chronic diseases, neurological problems, and cancers. He specialized in developing incapacitating biological agents and mastered the art of this new class of germ weapons that were nearly incurable and caused devious effects on the afflicted. In my recently published book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I walk the reader through the story of his career from the time he entered veterinary medicine in 1927 to his death in 1985.

In the book, I am able to link Traub to the Lyme disease spirochete and the cocktail of tick-borne diseases now spreading in the United States and abroad. But it goes further, I am able to demonstrate his discovery of the condition underlying many stealth, debilitating chronic diseases, coined immune tolerance, as the machinations for this new class of immunological weaponry, which he discovered with Lymphocytic Choriomeningitis Virus (LCM) in 1936. He contributed significant published research and findings on the science of these slow, chronic diseases and their infectious etiologies, but it was ignored by the public health system and only attributed to organ transplants. This was because they were intentionally trying to bury his work and all that it implied. It put a dent in their antibody and inflammation theory of disease, showing disease could be present without either antibodies or inflammation, but instead the polar opposite, as a chronic immunosuppression and reactivation of latent viruses in the central nervous system, brain, and organs, in other words, these agents turn the immune system and body against itself.

During his long career, he was able to show that certain lipid-like antigens could damage the immune system and cause lifelong infections that lacked outward symptoms like inflammation, lacked antibodies despite active infection, and spread virulent virus without any signs of disease. He discovered this condition in 1936 and it became the model for his new class of germ weapons. These mice would have active viral infections transmitted from the mother and be infected for life without antibodies or outward signs of disease, but later in life they would develop chronic neurological diseases and cancers, with the cancer rate eventually reaching 50%.

The infected mice would continue infecting their newborns through the infected mother, and the agent could maintain itself for many generations, getting more devious with each subsequent generation. It was a way to thoroughly hex the target nations because his agents were immunosuppressive and neurotropic, that is, they attacked the central nervous system and brain. This causes severe neurological disorders and mental illness to skyrocket. Attack the immune system, and you attack the life force of the individual, and chronic fatigue will tire and exhaust the afflicted to the point of incapacitation. Attack the brain of a population, and you attack the well-being and mental stability of that population. Violence and instability skyrockets, crime and drug use become commonplace. Exactly what we see today, in parallel to the epidemics of chronic disease and cancer.

Traub studied this condition his entire life and applied his germ weapons to cause the immune tolerance condition, and the accompanying neurotropic effects when viruses in the central nervous system reactivate and destroy the nerves, brain, and organs of the individual slowly and painfully. I cover the condition in other articles like The Dark Triad of Immune Tolerance: Chronic Disease, Mental Illness, and Cancer.

My book demonstrates how and why millions of people can be quite sick yet appear normal to a physician, with no abnormal blood work, no detectable antibodies, and no abnormal scans using the standard diagnostics available to physicians. These patients are then told there is nothing wrong with them, when in fact this is far from the case. My book conclusively demonstrates the machinery behind mystery diseases like chronic fatigue syndrome, myalgic encephalomyelitis, fibromyalgia, chronic Lyme disease, and beyond, explaining why they cannot get any help. This is the science they wanted to bury along with the life work of Erich Traub.

Traub also made a specialty of turning various animal diseases into human pathogens. It was all done without the need for modern genetic engineering technology, which I have explained in another blog post, Animal Passages & Biological Warfare: The Means and Methods of Bioengineering in the Days Before Recombinant DNA, showing that modern genetic engineering technology was not necessary or even desirable. Erich Traub, while being a virologist, was also a veterinarian and hid his secret biological weapons research was hidden under the cloak of veterinary problems and agriculture. It provided the perfect cover for the dirty business of biological weapons and he had mastered the art of creating stealth biological weapons and turning devious animal diseases into human pathogens.

In my book, I present Traub’s story for the first time, with in-depth analysis and a superior understanding of his scientific work and the conditions his weapons caused. I demonstrate how the combination of many infections from just one tick-bite caused complicated chronic diseases that disabled the immune system and caused a secondary neurotropic disease. I unravel the mysteries of Lyme disease, among other pathogens like Serratia marcescens which was then used in open-air tests by the U.S. Military and caused illnesses and deaths. I present his entire career from start to finish and how he becomes a doorway to so many other aspects of the story and the current epidemics of chronic disease, neurological disorders, mental illnesses, and cancers. I would also like to point out that he was producing these weapons for countries who asked for such weapons to be produced. It would be a mistake to think the blame can be placed on Traub alone, as he is but a doorway to the forces and powers that employed him and sought to use these weapons in the first place.

I highly recommend buying a copy and reading for yourself the story of biological weapons, including the life work of Erich Traub, presented like no other researcher has done until now. This book contains many answers that helpless sick people have been looking for, and why the healthcare system has failed them. The answers are in this book, revealed for the first time.

Buy your copy of The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, here: https://www.thesleeperagent.com/product-page/the-sleeper-agent

https://www.youtube.com/watch?v=X5RjvbI7CuE&t=163s

Nowadays, just about everyone has some kind of chronic health problem, whether it is considered auto-immune, fibromyalgia and joint pain, chronic fatigue, migraines, chronic headaches, brain fog, and many forms of mental illness which now run rampant in society. They are usually attributed to genetic factors or unknown origins, that is, doctors either say its bad genes or it 'just is.' They won't attempt to get to the root of the problem, they only attempt to mask the symptoms. But what if all of these health problems have a common origin? What if all of these disorders and syndromes are infectious in their etiologies and explainable, even in the face of normal blood work and scans?

In today's "evidence-based medicine" they would have you believe that there is absolutely no evidence that all of these issues are due to infectious disease. Worse, most of them won't even admit that things like chronic fatigue and many of the associated problems exist as anything but a figment of the imagination or "depression" since the tests, scans, and bloodwork usually will come back normal. At the same time, tests for infectious diseases will also come back negative. But yet, the person is infected, suffering, and definitely not imagining these symptoms. The tests come back normal for a reason, and it is not because the patient is imagining it, but rather because the tests used to assess the patient are incompetent.

This is entirely explainable and I will show that indeed, early German virologists like Erich Traub had already understood these mechanisms as far back as 1960, with the start of its discovery in 1936. Unfortunately, when it was coined 'immune tolerance' in 1960, it was awarded to two scientists who weren't even nominated together, and it was misleading in that they only applied this condition to the same condition brought on by organ transplants rather than infectious disease. It was a strange twist of fate that would do more damage to the Western public health than anyone could possibly imagine.

In my new book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I present for the first time, the existence of stealth biological weapons that target the immune system and cause slow, chronic diseases that lack detectable antibodies to the stealth bioagents, lack outward signs of disease like inflammation, stay clear from the blood, and attack the organs, lymph nodes, central nervous system and brain, causing chronic fatigue, low-grade encephalitis/permanent headaches, secondary neurological and psychiatric disorders, while causing cancer to skyrocket.

Imagine, if you can, stealth biological weapons that attack the core of your being, that do not show up in diagnostic tests nor show any abnormal blood work that doctors use to diagnose, and without the level of inflammation that doctors can see in scans or in person. The afflicted would be tormented and suffering from a very real disease, but the doctor would tell them they are not sick and see nothing wrong with the patient. This is precisely the result that these kinds of stealth biological weapons were designed to do, and it fries the immune system in the process. It is a certain condition known as immune tolerance, discovered by Erich Traub in 1936 with a virus called Lymphocytic Choriomeningitis (LCM). Accompanying the condition was a secondary neurotropic effect that attacked the central nervous system and brain. In my book, I present the story and work of Erich Traub who went to work modifying animal diseases to cause the same condition and turned them into human pathogens.

I show in my book, that after the Western countries were seeded with stealth biological weapons from directed bioterrorism by Stalin and the Soviet Union in the Cold War, along with those in public health, some having ties to communist front groups, using the same antigens that cause the disease, as vaccines, but do the same damage, and it is no coincidence that slow, chronic diseases are becoming the norm, along with mental illness, neurological disorders, while cancer continues to skyrocket.

Buy a copy of my new book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, that tells the story for the first time!

Buy your copy here: https://www.thesleeperagent.com/product-page/the-sleeper-agent

In my recently published book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I unravel the mystery of whether the Lyme disease spirochete was a biological weapon, and I was able to tie it directly to developments by the Nazis like Erich Traub and his colleagues during the Third Reich. I put forward reliable evidence to show precisely when he acquired the spirochetes and how it was developed, weaponized, and adapted to new animals it didn’t previously infect.

Traub learned how multiple, overlapping tick-borne infections suppressed the immune system and caused the disease condition known as immune tolerance, which I described in other posts like Immune Tolerance: The Basis of Slow Chronic Disease Accompanied by Mental Illness and Cancer and The Dark Triad of Immune Tolerance: Chronic Disease, Mental Illness, and Cancer. In my book, the entire story unravels the mysterious journey of Erich Traub’s life and career as a bioweaponeer for three different global superpowers.

Later in the book, I dispel the pathetic attempts by David H. Persing and Sam Telford in their Washington Post article, No, Lyme Disease Is Not an Escaped Military Bioweapon, despite What Conspiracy Theorists Say, with their attempt to discredit the idea that Lyme disease could have been a biological weapon, using misleading angles that stretch the truth to the point of falsehood, cite irrelevant arguments like the idea that genetic engineering technology wasn’t available yet or that Lyme’s week-long incubation period was too long to be an effective bioweapon.

Both are irrelevant points because long before modern genetic engineering technology was available, bioweaponeers like Erich Traub ran the agents through certain animals in serial passages to mutate the agent, adapt it to new hosts, among other things, and I explain this in my post Animal Passages & Biological Warfare: The Means and Methods of Bioengineering in the Days Before Recombinant DNA, and it is explained in further depth in my book. Secondly, a week-long incubation period is not that long, as Q Fever has an incubation period of 2-3 weeks and was among the biological weapons held by the military in the American biological weapons stockpile. Psittacosis (ornithosis/chlamydiosis), another biological weapon in our stockpile, has an incubation period of 5-14 days. His argument there is completely invalid.

Telford and Persing go on to cite incredulous evidence to say that it was found in mouse tissues from 1896 in Cape Cod, because of his finding small fractions of genetic material from the outer surface protein in the mice. However, a tiny fragment of genetic material from the outer surface protein does not in any way prove an infection with Borrelia burgdorferi because plasmid DNA is variable and changes all the time, not to mention, it is cross-reactive to other pathogens and viruses, namely vaccinia virus, and Persing says so in his paper, Target Imbalance: Disparity of Borrelia burgdorferi Genetic Material in Synovial Fluid from Lyme Arthritis Patients.

Also, Persing and Telford cite another paper showing it was found in ticks collected from 1945-1951, which only reinforces the story you will read in my book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. It is also interesting to note that Richard Marconi from the Rocky Mountains Laboratory published a paper demonstrating that the set of primers Telford and Persing were using were not a reliable set of primers and therefore could not be trusted as evidence for the argument they were trying to make, and cites their paper as one of those using these unreliable primers to prove the DNA was able to demonstrate an infection with Borrelia burgdorferi. In the tick samples from 1945-1951, they at least tested for spirochete DNA along with the outer surface proteins (plasmid DNA), while the samples of mice tissue from 1896 were only testing for tiny fragments of plasmid DNA and not the actual spirochete DNA. But let’s say the tick samples from 1945-1951 were actually infected with Borrelia burgdorferi, it would only reinforce the story I have demonstrated in my book.

Clearly, their article was just another pathetic example of propaganda to discredit something that actually has merit, and this will be clear when you read the story in my book, and see the evidence for yourself. Without giving too much away, I highly recommend buying and reading my new book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, and walk with me through the diabolical labyrinth of Erich Traub and the stealth weapons of biological warfare. Learn about how he became well-versed in tick-borne diseases like the Lyme co-infections (Babesia, Bartonella, Ehrlicia, etc.), acquired the spirochetes, weaponized them during the war in Germany, gave them to the Soviet Union, and brought them to America, updating them once more.

John J. Loftus, who wrote America’s Nazi Secret, was the first to expose the Lyme disease connection to biological warfare, in 1982, and he made the revelation that they were spread by ticks before it was even acknowledged by scientists, a year later being confirmed by the biodefense specialist Willy Burgdorfer from the Rocky Mountain Laboratory. John Loftus wrote the forward to my book, and endorses the story I have presented, and his biodefense sources with Q clearances have said that my work is spot on. Loftus became a good friend of mine when I started writing the book in 2017, and he endorses my story as accurate and true according to all the intelligence his sources have relayed to him when he was a pro bono attorney for those in the intelligence community working to get other damning stories declassified after he exposed Operation Paperclip on 60 Minutes in the 1980s.

Therefore, he will tell you in the forward that much of modern history has been classified. He revealed in his 1982 book that most of the biological warfare files have been shredded, and when you read my book, you will understand why they would want this story to disappear and tried to get rid of all the evidence. But shredding the majority of files was not enough to stop a determined, skillful researcher like myself, sick with Lyme disease, to unravel the mystery using many other sources of evidence. They wanted this story to disappear and remain buried, but this book will walk you through the story and you shall see for yourself…

Buy your copy of The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, here: https://www.thesleeperagent.com/product-page/the-sleeper-agent

https://www.youtube.com/watch?v=Bc039rWiw6k&t=693s

In my newly released book on the history of stealth biological weapons, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I explain the concealed manner in which contemporary biological warfare programs have developed and operated for the last century – secretly – using the cover of benign medical and agricultural research and maintained in such a way as to be indistinguishable from defensive or benign scientific research. I discuss not only how it is done, but also why it is done, so that the uninitiated can grasp it with ease.

First, let it be known that in World War I, the use of unconventional weapons like chemical and biological weapons by Germany left a horrifying imprint upon the memory of those who witnessed the grisly deaths caused by chemical weapons, and the use of germs to sabotage horses used for military and medical purposes caused such a disruption that Germany was sanctioned by the League of Nations resulting in the Treaty of Versailles, a treaty that enacted heavy fines against Germany that were economically crippling and outlawed them from maintaining a military on their homeland. It took Germany over 92 years to finish paying their debt from these sanctions and paved the way for the rise of Nazi Germany with the aid of the Soviet Union.

The League of Nations made an example out of Germany, and gave a harsh reminder to other nations, what would happen to them if they decided to follow in the same footsteps as Germany. It was not enough to prevent the global superpowers from continuing to develop such weapons, but it changed the manner in which it was done. Because no one wanted to end up like Germany, they found ways to hide the research and development of such weapons under benign covers like agricultural, medical, and general scientific research that would be indistinguishable from benign research. It allowed such research to be disguised and hidden not only from their own civilian population, but also from prying enemy eyes. Germany’s overt use of such weapons in World War I brought them a very bad reputation and from that point forward, chemical and biological warfare was seen as a dirty business and most countries would vehemently deny engaging in it, despite the fact that they were all doing it. It is for this reason you will never ever hear of a weapon being called a weapon on paper or in discussion, they simply do not make this mistake.

As a result of these special unconventional weapons used by Germany in World War I, the League of Nations held the 1925 Geneva Convention with international treaties enacted to ban the use and stockpiling of chemical and biological weapons. Most if not all countries were not abiding by the treaty in the decades to follow and several biological warfare programs of global superpowers became known and the Geneva Protocol of 1925 did not offer much clarification on research to defend against biological warfare. As a result, a revision was made and a new treaty was put forth in 1972 called the Biological and Toxin Weapons Convention (BTWC), and this new treaty allowed biological warfare research for defensive purposes.

As a result of the BTWC of 1972, many offensive biological warfare programs actually expanded because they would be covered legally if they said it was simply "defensive research," so it gave them a protective blanket to cloak their nefarious biological warfare research as defensive work, and they could get away with far more offensive work than in the days when the 1925 Geneva Protocol Treaty was the rule of thumb.

These factors and more are explained in greater depth in my recent work, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, available now. Begin your education and initiation into the secret history of stealth biological weapons and their effects on health, equally learn why their alleged vaccines can impart the very same illness as those developed as weapons.

Get your copy here:https://www.thesleeperagent.com/product-page/the-sleeper-agent

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https://www.youtube.com/watch?v=rMXQVaXCGhQ&t=443s

In my recent book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I cover in the first two chapters, the early developments and uses of biological weapons from their primitive use in older times up to the days of World War I, and I put special emphasis on the devastation caused by the 1918 Influenza, erroneously called the “Spanish” Influenza, or “Spanish Flu” for short. It was only coined the “Spanish” flu because at the time of World War I when it began to spread, the United States had censored the press from reporting on it under severe penalties to prevent panic among the soldiers who were enlisted or about to be drafted into the military and sent to war. This was done not only in America but in many additional countries involved in the War effort.

The point of origin for the 1918 Influenza has been documented as Fort Riley and Camp Funston, in Kansas, starting in March 1918, just a month after the Rockefeller Institute finished up testing experimental meningococcus vaccines on soldiers. While I make no definitive claims about the vaccine being the cause of the 1918 Influenza, I explain in my book how the injections would have certainly enhanced the Influenza spreading in that location among soldiers about to be shipped overseas to the frontlines. I simply show how meningococci can suppress the immune system and allow the circulating virus a perfect environment and opportunity to rapidly mutate to reach a very high virulence, especially in soldiers tightly packed in ships sent overseas to war.

But more than this, I also point out the relationship between the meningococcus vaccine and the German biological sabotage program of 1914, where German Agents setup shop in the United States to covertly infect military and medical horses around the country with such germs as glanders (Burkholderia mallei) and anthrax (Bacillus anthracis). I point out that horses were a major target at the time, not just because of their use in military cavalries, but also because horses and horse tissues were in widespread use to produce serums and vaccines (as broth for growing cultures of meningococci often used horse tissues) intended for human use. I show how the 1918 influenza virus mangles the immune system and invites secondary bacterial infections to deliver the deathblow. I make the case that the events surrounding the German biological sabotage program provided the perfect environment to aid and abet the 1918 Influenza to bring the global devastation it did.

But this is not all, in these early stages of germ warfare, we find British Intelligence overlapping and having infiltrated the German sabotage program, secretly giving the Germans a little help to make the program more costly for the Americans, who were supposed to be their allies! Why British Intelligence would help the Germans attack their American allies would seem virtually implausible to the average person, but the first chapter of my book takes the reader back even further to primitive biological warfare employed by the British against American Native Americans and aborigines in Australia during the early days of American and Australian colonization, where smallpox was used as a weapon to wipe out tribes that posed a threat to the British colonies.

These early instances of primitive biological warfare are not theory but established facts. Moreover, the British even used smallpox as a weapon in attempt to defeat the American Continental Army with quoted correspondence by the First American President and then-General, George Washington, discussing the deliberate use of smallpox as a weapon against the Continental Army during the early days of the United States of America. Again, Washington is directly quoted on the British use of smallpox as a weapon against the Continental Army, establishing its factual context.

This inevitably leads us to review further epidemics in the following century where suspicious British activities brought the United States and Australia serious epidemics of contagious bovine pleuropneumonia (Mycoplasma mycoides) just years apart, while also leaving a suspicious context surrounding the Irish potato famine caused by the potato blight fungus (Phytophthora infestans), which later became an established biological warfare agent used in anti-crop warfare and employed by the British in World War II.

Early in the book, the reader is given an in-depth look at the factors that led up to the 1918 Influenza, with horses and cattle being targeted and deliberately infected by the British and blamed on the Americans, while Germany began to suspect hostile actions by the United States, and this set the pretext of antagonism between Britain, Germany, and the United States, that eventually led up to the First World War and pulled Russia into its nefarious activities, and because of the devastation witnessed on the Russian side from the 1918 Influenza and the typhus epidemics, it was a testament on the effectiveness of using germs as prospective weapons to fight future wars.

After the world witnessed the devastation caused by the 1918 Influenza, the factors that provided its unique environment and the biological components involved would later become the model to emulate in future research developing effective biological weapons. It sheds light on the viral and bacterial synergy involved in the unique and fatal outcomes of respiratory viruses and their use as weapons. In further depth, we review the claim by Soviet Intelligence that the 1918 Influenza was a weaponized avian influenza developed by the British and used against the Russians. This and so much more is covered in great depth in The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare.

Buy your copy of The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, to learn the astounding fact of how widespread the use of biological warfare was by the days of World War I, along with its primitive use since the formation of the United States of America as far back as 1763! Read with astonishment, direct quotes from the first American President on the use of biological weapons against the Continental Army by the British, and learn what has been buried in obscurity for so long – the prevalence and reality of biological weapons – as special weapons of war and biological terrorism! This book details out the hidden history and esoteric art of germ weapons like no other book on the subject has done, until now!

Get your copy here: https://www.thesleeperagent.com/product-page/the-sleeper-agent

https://www.youtube.com/watch?v=7KiRJVVQ9yo&t=943s

In today’s day and age, very few are aware just how successful biological warfare became in the quarrels between global superpowers. Very few know that in the Cold War, biological warfare became the favored warfare, and in 1938 Stalin declared it was the weapon to fight future wars. In fact, stealth bioterrorism was employed again and again by the Soviet Union against the West after the defeat of Nazi Germany. In my recent book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I walk the reader through the labyrinth of stealth biological weapons and their use in secret acts of sabotage. This was the most preferred way of attacking with biological weapons, through intelligence channels and embedded spies in the science and academic circles, working in the biodefense programs, who could carry out secret acts of sabotage against the West.

The reason biological warfare was preferred over any other warfare was because these are the only kinds of weapons that can be used and blamed on nature as a natural event and deny it was a deliberate act at all, while still having all the advantages of a directed attack. It brought with it plausible deniability. Aside from catching the saboteur in the act, the target nation would have a hard time proving definitively that the outbreak was an act of bioterrorism, or if it actually was a natural event. Either way, the damage gets done, with the attacking country able to freely deny it was an act of bioterrorism. The target country would be hesitant to retaliate if they could not prove the outbreak was an act of bioterrorism. You must know, that attacking a nation brings war if it is seen as a deliberate attack, but with these biological weapons, the ability to deny the attack is there, and in turn, without hard evidence of an attack, a country will be hesitant to retaliate.

Biological sabotage was the method of attacking enemy nations and it was used very effectively thanks to spies and saboteurs embedded in the target country. In my book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, I detail the history of stealth biological weapons and the ongoing biological war between global superpowers. Using government documents and other legitimate sources of evidence, I show how major bioterror attacks were unleashed on the West just after World War II, and how the biodefense open-air simulant testing activities using bacteria thought harmless, were sprayed in the air over populated areas, as well as using insects, thought uninfected, were actually weaponized and served as secret acts of sabotage. This was an embarrassing blunder very few are even aware of, and the powers that be were hoping this would fade away into obscurity, but instead I hope to educate the reader and show how these activities are still going on today!

However, the more people educate themselves and the more people understand the mechanics of this war and how it secretly waged, the better chance of putting an end to it, because today, many attacks can be easily hidden under scientific and academic research activities, experimental testing, and so on. Foreign governments are invested in its use through spies posing as scientists, professors, and biodefense specialists, with the sole purpose of hurting innocent civilians in the targeted country.

In 2005, Ex-KGB Alexander Kouzminov wrote a memoir Biological Espionage: Special Operations of the Soviet and Russian Foreign Intelligence Services in the West, detailing out some of the operations of directed bioterrorism against the West, coined “Day X” and talked about just how many spies they had in the United States and Western countries.

I discuss many of Kouzminov’s revelations in my book, and I mention the unsettling fact that vaccines were also named as a major target for clandestine bioterrorism. Buy your copy of The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, and learn the secret history of stealth biological warfare and its ongoing war that still maintains itself today.

Buy your copy here: https://www.thesleeperagent.com/product-page/the-sleeper-agent