Immune Tolerance and Slow-Virus Disease: Skeletons in the Closet of Western Science & Public Health
By: A. W. Finnegan
Abstract: The mechanisms of chronic disease had been discovered as far back as 1936 by German Virologist Erich Traub, and later termed immunological tolerance, or immune tolerance, for short. Unfortunately, what could have added voluminous contributions to the nature and science of chronic disease and its infectious etiology was occulted in 1960 and attributed to organ transplants. The fields of immunology, vaccinology, and infectious disease were severely and negatively affected by the masking of immune tolerance, and public health has suffered irreparable damage. The spread of chronic disease and para-infectious injury has been steadily increasing since the early 1950s and beyond. Western prophylactics and over-vaccination have added significant burden to already overwhelmed immune systems and vulnerabilities in manufacturing have greatly contributed to exacerbating the problem. The secondary neurotropic effect on society has been disastrous and far-reaching. The cumulative effect of incomplete science and immunology on society may be unfathomable in scope.
By: A. W. Finnegan
Abstract: The mechanisms of chronic disease had been discovered as far back as 1936 by German Virologist Erich Traub, and later termed immunological tolerance, or immune tolerance, for short. Unfortunately, what could have added voluminous contributions to the nature and science of chronic disease and its infectious etiology was occulted in 1960 and attributed to organ transplants. The fields of immunology, vaccinology, and infectious disease were severely and negatively affected by the masking of immune tolerance, and public health has suffered irreparable damage. The spread of chronic disease and para-infectious injury has been steadily increasing since the early 1950s and beyond. Western prophylactics and over-vaccination have added significant burden to already overwhelmed immune systems and vulnerabilities in manufacturing have greatly contributed to exacerbating the problem. The secondary neurotropic effect on society has been disastrous and far-reaching. The cumulative effect of incomplete science and immunology on society may be unfathomable in scope.
In 1960, Western science and public health systems began their long, treasonous descent into a one-sided, misleading paradigm of immunology and infectious disease. This step not only ignored the science of this discovery, but went as far as to mask the infectious origins of what is known as "immune tolerance" by giving the Nobel Prize to two scientists, Burnet and Medawar, not even nominated together, and attributing the condition to be restricted to the same condition seen in organ transplants. [1] This scientific discovery which underlies chronic disease was actually discovered by German researcher Erich Traub starting in 1936 with the virus of Lymphocytic Choriomeningitis Virus (LCM), but his contribution was not publicized or credited to Traub, it was instead given to other scientists having to do with something more obscure. [2] This was an act that would bring untold suffering and unnecessary harm for future generations, because it was at this point that science and public health began to turn their backs on a large portion of immunology and one-half of the entire spectrum of disease- chronic disease- and medical progress has been moving nearly in reverse ever since. [3]
This spectrum of disease has been covered in layers of scientific fraud and unnecessary controversy. [4] This act of denying the infectious processes of immune tolerance many years ago, was a pivotal moment in which profiteering and ego became more important than the easing of human suffering, because if the science of immune tolerance had been acknowledged for what it was and the implications that it implied, those in the established science and public health systems would have been forced to rethink the entire paradigm of immunology, vaccination, inflammation, and the very nature of disease itself. This would indicate that the act was done, not just because of the controversial background of its German pioneer, Erich Traub, but because of conflicts of interest involving profiteering and the reputation of establishment science and Big Pharma.
Immune Tolerance, as I will show, is the term that denotes the condition that underlies most if not all of chronic disease, a relapsing/remitting yet progressive condition that ties autoimmune conditions, genetic disorders, endless syndromes, and mental illness to para-infectious mechanisms, through a disrupted immune system and neurotropism, by the proliferation and persistence of a disseminated viral syndrome, where latent viruses already present in the body will reactivate and turn on the body, making the bulk of the condition itself. [5] [6] [7] [8] It is akin to turning one’s own microbiome against itself, and no doubt, it is why so many people have so much trouble getting well. [9] This process and proliferation of antigen makes it hard to absorb and take in nutrients, oxygen, and the like, [10] because there is a state of balanced parasitism, and the person will tend to operate at a very low capacity, being malnourished and highly diminished vitality. It is like being somewhat choked out or suffocated at the cellular level. [11]
Immune tolerance will often present without any outward symptoms, but the effect is still damaging due to the parasitic nature of the para-infectious invasion which remains in the body, and active infection can be entirely present without antibodies. [12] Oftentimes this balanced parasitism will turn in favor of the parasitism of virus and antigen. Erich Traub and his mentor Karl Beller noted this in his studies of an AIDS virus of horses, Equine Infectious Anemia Virus (EIA), and the resultant condition was not a true immunity:
It is therefore very questionable whether this is a true immunity. The term "prämunity", which originates from French and becomes more and more natural in German terminology, would probably be more appropriate here. In human and animal protozoal diseases, after the survival of the clinical phenomena existing equilibrium state between parasite and organism, in which the latter is usually resistant to a new infection. Due to damaging influences on the body, this state of equilibrium can change in favor of the parasite. Similar observations were made in [infectious anemia]. [13]
As a result of this truly immoral act of burying the science of immune tolerance, a harmful butterfly effect would take root and branch into every facet of life, every angle of health would be significantly affected, to such an extent that it would change the course of history in untold, unprecedented ways. [14] This fraud would have a cumulative effect that would only grow in intensity over the years, each decade would become more unstable, and to cover these tracks, more unsound explanations would have to be layered over it, and the more out of line with Truth reality became, the more chaotic and unstable its consequences would follow in public health. If there is any hope of fixing this diabolical treason, we must revisit the past, and recall the events in which it took root...
Traub’s Discovery of Immune Tolerance
In 1935, a German student studying on a scholarship at the Rockefeller Institute, Erich Traub, was studying the reactivation of latent viruses in equine encephalomyelitis and swine fever virus (hog cholera), [15] after transmission studies with Richard Shope in Iowa on the pseudorabies virus, a swine herpesvirus unrelated to rabies, [16] after which Traub began a series of experiments in mice, where he was attempting to reactivate a latent virus to cause an epidemic in the mouse colony at the Institute. He injected the mice intracerebrally with foreign proteins or antigen suspended in sterile bouillon, and within short order, an outbreak ensued and infected most of the other mice in the colony, though they all had been otherwise healthy mice before the experiment:
During recent work with the viruses of equine encephalomyelitis and hog cholera an infective agent was obtained from white mice which was pathologically and serologically distinct from both viruses. Its origin was not definitely known, but it seemed likely that the natural host of the agent was the mouse, in spite of the fact that in our mouse colony no disease had been previously recognized. In an experiment designed to trace the origin of the infectious agent, 60 five-week-old, healthy-looking mice from our colony were each given an intracerebral injection of a small amount of sterile bouillon. Fifty-one of these mice showed no evidence of illness during the three weeks that they were under observation. Four died in from 3 to 13 days following the inoculation, and three were killed on from the sixth to the eighth day when they showed symptoms similar to those observed in the mice inoculated with the unknown agent. On the sixth day two additional mice that showed photophobia but no other symptoms were killed. From one of these mice no material was obtained for inoculation, but bacteriologically sterile suspensions of the brain of each of the other eight when injected into guinea-pigs caused symptoms which could not be differentiated from those produced by the original material. This experiment, together with others, suggests that the infectious agent is carried by apparently healthy mice in our colony and that symptoms may be brought out by the intracerebral injection of foreign protein. [17]
The outbreak, however, was not just restricted to the mice, because soon some of the lab technicians and animal keepers contracted the virus and had to be hospitalized, infected with this new virus, which they called Lymphocytic Choriomeningitis Virus (LCM):
In 1935 an epidemic of meningitis of a special type (acute lymphocytic choriomeningitis) broke out in the mouse colony in Princeton. Erich Traub recovered a virus to which he gave several years of intensive study before he left the Institute in 1938. [Interestingly], one of the Princeton staff contracted this disease during the mouse epidemic and was studied at The Rockefeller Institute Hospital by T.M. Rivers and T.F.M. Scott, who isolated from him a filtrable agent identical with Traub’s. Traub’s observations show that the mouse is the natural host of this potentially serious infection, which, fortunately, only occasionally causes illness in human beings. The virus, kept alive in mice by healthy carriers, is acquired by infant mice from their mother while still in utero or shortly after birth. Usually remaining latent, like many other viruses it is occasionally awakened to virulence by some accidental circumstance, causing a disease which spreads with epidemic rapidity. [18]
This was transmissible and able to spread from animal to human. Traub studied this virus in the colony for several years and noted its persistence in the colony, establishing acute and chronic infections, which set the discovery of immune tolerance in 1936. [19] He noted congenital transmission from mother to newborn, where the virus would persist and become increasingly more silent in the colonies, [20] but later in life the infected stock would present with blood cancers and leukemia, [21] as well as chronic, progressive neurodegenerative diseases in what was later termed early and late onset disease, [22] resembling debilitating chronic conditions that progressively destroyed the central nervous systems of these mice as they got older. [23] The study would be some of the early models of progressive neurodegenerative chronic diseases which would later become so prevalent in Western countries. [24]
Traub’s seminal work on LCM virus became the model of an immunosuppressive, relapsing chronic disease, which would become so prevalent in Western societies in later generations. It was termed immune tolerance, in that the body’s immune system was not immune to the virus, as in actively neutralizing it, but rather tolerized to the virus, meaning it would not respond to it, little to no antibodies would be produced after the initial infection, and the virus would be able to continue its replication and spread, establishing in the infected subject a slow-virus disease. [25] The slow-virus disease meant that the disease took a much slower, chronic course. The mother would transmit the virus to the young, and the young would be born tolerized to the virus, not showing outward symptoms but having a slow, chronic infection which later in life would turn to chronic disease and result in neurodegeneration, lymphomatosis and cancers. [26] [27]
Traub noticed that antibodies were minimal in the infected colonies, even though they were carriers and shedders of active virus. However, when the rest of the stock was more or less immune tolerant, it would be hard to tell this was the case, but the effect could be spotted if these mice were put into an uninfected colony. [28] Another phenomenon observed in the infected stock, was that the virus only remained in the blood for several weeks and then disappeared from the blood, taking to organ, tissues, brain, and some of the secretions and excretions. [29]
What Traub’s studies in LCM taught us was that, first, there were such thing as infections that failed to produce noticeable antibodies, making today’s diagnostic methods and approaches to infectious disease somewhat meaningless. [30] If viral infections that fail to produce antibodies were diagnosed through the detection of antibodies, it would miss these cases and falsely declare them negative for infection. Also, with viral infections known to clear from the blood on top of the little to no antibodies produced, serological testing was not sufficient to confirm infection. This would indicate that the state of surveillance for many infectious diseases could be vastly underestimated and incompetent.
Secondly, the process in which Traub was describing immune tolerance, was actually the way that vaccines were imparting their so-called immunity, they were not necessarily neutralizing virus from the body, the body was rather being tolerized to certain antigen. [31] It would trade the acute expression for a slow, chronic course, but came with neurologic side effects. [32] The antibodies produced by vaccination were only initially generated, and eventually would just fail to produce a response when tolerance was achieved. The vaccine then does not induce immunity, as in neutralizing the virus from the body when future infection is contracted or present, it just tolerizes the immune system not to respond to antigen, and thus, the shedding of virus still occurs. [33] Live virus vaccines are claimed as setting up harmless, latent infections, but rather, these are slow-virus infections, and the harm can still be destructive in the end, but the course is much slower, while reactivation can also occur. [34] Tolerization is not a harmless process and the condition brings a multitude of other complex and chronic health problems, [35] such as progressive neurodegenerative diseases, [36] autistic spectrum disorders, [37] gastrointestinal problems, [38] secondary opportunistic infections not commonly seen or understood by the average physician or even infectious disease specialist. [39] This was the trade off to acute disease for most people with the introduction of vaccinations. [40]
There were still some cases whose immune systems mounted a more robust immune response to these class of antigens, remaining with the acute presentations, also higher allergic response to vaccines with these antigens. It was a small percentage of roughly 15%, while 85% presented with immunosuppression. Lyme disease was one example of a pathogen that induced this immunosuppressive condition and the problems associated with it. This disease also showed that this 85% tested negative to the disease while actively infected, as the antibody response was minimal. The other 15% had a more noticeable disease but these cases were also more responsive to antibiotic therapy. The same agent produced a variable response in different ratios of people with variable HLA makeup. There was even a certain small percentage appearing to present with both outcomes simultaneously. [41]
Vaccines like the polio vaccine, contaminated with adventitious virus like SV40 virus, is an example of a virus that mirrored the LCM virus. [42] Many of the human herpesviruses like Epstein-Barr Virus, HHV-6, Herpes-simplex, were also viruses that could act much like LCM virus when reactivated to active form. [43] In many ways LCM served as an animal model of the herpesviruses in humans. [44] Vaccines were oftentimes contaminated with adventitious animal viruses that mirrored LCM virus, [45] and the lipoprotein antigens used in vaccines could also cause the effect of reactivating latent viruses in its human recipients, [46] much like Traub’s experiment in mice with foreign antigen injected into the brain. [47]
I. Immune Tolerance & Vaccinations: A Forecast of Unforeseen Complication and Crisis
There are serious issues of concern in attempting to mass immunize or compulsively-immunize a population with varying degrees of immunosuppression from stealth infections, [48] [49] [50] along with failure to detect adventitious virus, that is, hidden viruses and pathogenic microorganisms within the material as contaminants in commercial vaccines and gene therapies, which has not been given a significant level of attention, but presents a significant danger to those receiving them with the aforementioned dilemmas left unaddressed, and common people are paying the price with their livelihood in such unfortunate situations. [51] Unfortunately, this topic has become so laden with controversy and heated debates, that very few will speak freely about it. However, it must be addressed one way or another, because safety comes before reputation, if one is truly a health practitioner. [52] There are two main factors involved that make the overall picture a serious problem in regards to this picture, where stealth infections have proliferated the population causing a crisis of both chronic disease and mental illness. The two main points in the risk of immunizations in the Western countries are:
a. Stealth Infections and Immune deficiencies.
a. Stealth Infections and Immune deficiencies.
Those already dealing with one or several stealth infections causing immunodeficiencies, immunosuppressed at the time of vaccination, and the immune response is poor or suboptimal, giving latent viruses within the host or vaccine material itself a chance to revert to active virulence. [53]
When a child or individual is overburdened by stealth, subclinical viral infections at the time of birth, born immune tolerant through congenital transmission, along with the older age groups who have picked up several infections in life such as the arthropod-borne diseases, hepatitis, and so on, the stacking of additional immunizations present a dilemma and danger to the public. [54] [55] There is very little done to check a child for immunodeficiencies at the time of immunization. Blood work is likely to appear normal, without antibodies to the infections, and thus, declared healthy. Traub’s work on LCM virus shows that the virus would pass through generations of mice, with the virus gaining momentum with each subsequent generation. [56] This same picture could be playing out in the population today. The rates of chronic disease, autism, cognitive and behavioral health problems, [57] [58] have reached an all-time high in Western civilizations, yet have the highest rates of immunization. [59]
Even so-called non-infectious antigen disseminates to the brain and CNS, [60] [61] causing cognitive difficulties, [62] arthritis and fibromyalgia. [63] Essentially, it appears we are trading acute diseases for chronic diseases; especially disseminated slow-virus infections through the reactivation of latent herpesvirus. [64] Compounding this problem, the number of immunizations a child needs to have just to attend school are significantly higher, and growing. [65] The compulsory vaccine practices of the West are essentially fanning the flames of a complex picture of immune tolerance and systemic proliferation of many stealth infections circulating the environment. [66] [67]
Stealth infections are evading standard medical diagnostics for infectious disease, little to no antibodies despite circulating virus or pathogen, the doctors see no clinical symptoms and designate them healthy. [68] Next, they suggest several immunizations, such as influenza, meningococcus, pneumonia, and so on. [69] These antigenic and live virus vaccines add significantly more burden on the individual’s immune system, with injurious, and in some instances deadly consequences. [70] If we continue this path, the problem will get exponentially more complex and problematic for the public health system, [71] already overwhelmed by the massive rise in chronic diseases, [72] mental health problems, [73] and so on.
Risks associated with immunizing an already overburdened immune system poses a very real danger. Researchers out of John Hopkins University Paul Auwaerter et al., published Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue, whereby an infant was killed by a vaccine strain of measles after its immunization, reflecting the mechanism laid out within this work:
However, fatal infections have been documented in immunodeficient children vaccinated with these strains (1, 12, 14, 15). The symptoms of infection occur many months after immunization, and the viruses isolated are similar to the original LA vaccine (1, 15), 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. [74]
A second, more indirect manner in which vaccine viruses may revert to active form, is by transmission of arthropod diseases after bites from ticks, mosquitoes, and other insects, which Traub had revealed in his 1939 thesis on immunity against viral disease, with the classical horse-sickness as an example:
In contrast to the neurotrophic yellow fever virus in monkeys, the neurotropic horse-sickness virus in an intracerebrally-vaccinated horse caused only a febrile temperature increase, but no encephalitis, while producing in mice always fatal encephalitis. The virus circulates in the blood of the horses during the fever period, which may be a drawback in that the horse sickness is most likely transmitted by blood-sucking insects; which is not guaranteed that the vaccine virus in the body of the presumed recipient cannot be transformed back into the original agent. However, this risk should be lessened by the fact that the vaccinations are carried out in a season in which blood-sucking insects do not occur or only in small numbers. [75]
The herpesvirus group, which includes 8 predominant forms, including Herpes-simplex (HHV 1, HHV-2), Varicella Zoster Virus (VZV, or chicken pox, HHV-3), Epstein-Barr Virus (EBV, as HHV-4), Cytomegalovirus (CMV, as HHV-5), Human Herpesvirus 6 (HHV-6), Human Herpesvirus 7 (HHV-7), Human Herpesvirus 8 (Kaposi’s Sarcoma-associated Virus, as HHV-8) is latent in most if not all human beings in one of the aforementioned forms. EBV and Herpes-simplex tends to be the most common of the herpesviruses seen, followed by VZV and CMV. The herpesvirus family can be neurotropic and greatly contribute to the neurological disorders commonly seen today, as laid out in a publication, Herpesvirus Infections of the Nervous System, by two researchers of neurological diseases in human beings:
RECENT FINDINGS: As more patients are becoming therapeutically immunosuppressed, human herpesvirus infections are increasingly common. Historically, infections with human herpesviruses were described as temporal lobe encephalitis caused by herpes simplex virus type 1 or type 2. More recently, however, additional pathogens, such as varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 have been identified to cause serious neurologic infections. As literature emerges, clinical presentations of herpesvirus infections have taken on many new forms, becoming heterogeneous and involving nearly every location along the neuraxis. Advanced diagnostic methods are now available for each specific pathogen in the herpesvirus family. As data emerge on viral resistance to conventional therapies, newer antiviral medications must be considered.
SUMMARY: Infections from the herpesvirus family can have devastating neurologic outcomes without prompt and appropriate treatment. Clinical recognition of symptoms and appropriate advanced testing are necessary to correctly identify the infectious etiology. Knowledge of secondary neurologic complications of disease is equally important to prevent additional morbidity and mortality. This article discusses infections of the central and peripheral nervous systems caused by herpes simplex virus type 1 and type 2, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6. The pathophysiology, epidemiology, clinical presentations of disease, diagnostic investigations, imaging characteristics, and treatment for each infectious etiology are discussed in detail. [76] The herpesvirus group of viruses are not limited to human beings, but are found in nearly all animal species. Many diverse animal tissues are used to produce vaccine material, which brings us to the second factor of major concern in the problem of para-infectious and post-vaccinal encephalitis:
b. Contaminants (adventitious or latent viruses, Mycoplasma, Toxoplasma, Acholeplasma, fungal and bacterial pathogens, etc.).
Commercial vaccines with pathogenic contaminants present in the vaccine material can produce a suboptimal immune response following the immunization, with latent viral contaminants concurrently inherited by the recipient, [77] resulting in immune deficiency or encephalitis, [78] giving the vaccine material an opportunity to reactivate and regain virulence, [79] especially live vaccines, which then circulate and shed from the body by their secretions and excretions, transmitting the pathogen to circulate the surrounding environment and those within close proximity to the individual. [80]
Contaminants in commercial vaccines is not a new problem. [81] It has been a thorn in the side of vaccine manufacturers all along, who have continuously been plagued by contamination in batches of vaccines already on the market circulating widely. For instance, Salk’s inactivated polio vaccine (IPV) was circulating and given out widely to millions of Americans and Western countries, but took five years before they discovered the vaccine was contaminated by several viruses, such as SV40, and additional polyoma viruses. [82] The estimation of those potentially infected was more than half the population, and close to 100% in some age groups, stated by NIH and John Hopkins researchers in Reviews and Commentary Human Exposure to SV40: Review and Comment:
Highly reliable information is available on the numbers and age distribution of the population immunized with inactivated poliovirus vaccines. These data were collected in yearly national household sample surveys conducted by the Bureau of the Census, in collaboration with the Communicable Disease Center (64). A summary of their report for the September, 1961 survey (51) is given in table 2. Over 98 million people, or 62 per cent of the population, had received one or more doses of the vaccine during the period when a proportion of the vaccine was contaminated with SV40. In 1961, potentially contaminated vaccine had been administered to almost 90 per cent of individuals under 20 years, 60 per cent of those 20-39 years old and 19 per cent of those 40-59 years old. [83]
Later in the report shows higher cancer rates from those born to mothers who had the polio vaccine, mirroring Traub’s studies of LCM during his Rockefeller years, as the virus is passed continually through generations:
Heinonen et al. (74) have recently reported a higher incidence of malignancies in children born to mothers who received inactivated poliovirus vaccine during pregnancy. In a prospective study of over 50,000 pregnant women between 1959 and 1965 (Collaborative Perinatal Project of the National Institute of Neurological Diseases and Blindness), 24 malignancies in their newborns were detected in the first 4 years of life. The rate of malignancy was about two-fold greater in children born to mothers immunized during pregnancy. [84]
These adventitious or hidden viral contaminants are potentially carcinogenic, especially when reactivated from latent to active infection. Even after the problem was discovered, they were not able to rid the vaccines of these contaminants, as Konstantin Chumakov et al., stated in a paper, Some oral poliovirus vaccines were contaminated with infectious SV40 after 1961:
Inactivated poliovirus vaccine (IPV) and live oral poliovirus vaccines (OPV) were prepared in primary cell cultures derived from rhesus monkey kidneys. Studies of these vaccines led to the discovery of a new virus called SV40 in 1959. This DNA virus caused vacuolization of green monkey cell cultures and was found to be highly oncogenic in hamsters (reviewed in refs. 1, 2). It was found that SV40 was endemic in rhesus monkeys. For this reason, the rhesus kidney cell cultures used to manufacture poliovirus vaccines as well as some seed stocks of poliovirus contained infectious SV40. (2–5). Therefore, the early batches of OPV contained infectious SV40 (3–5). Because formaldehyde treatment used to prepare IPV failed to completely inactivate SV40, some batches of IPV contained infectious SV40 (2, 4). As a result, it has been estimated that > 100 million people in the United States and many more worldwide received potentially contaminated vaccines prepared during the years 1954 to 1961 (2). [85]
This problem is still plaguing the manufacture of commercial vaccines, with inadequate testing, or contamination that occurs later in the vaccine material. [86] Many papers have been written in recent years discussing this dilemma. Furthermore, many of these animal virus contaminants are oncogenic viruses or immunosuppressive retroviruses like avian leukosis virus, discussed in Evidence of avian leukosis virus subgroup E and endogenous avian virus in measles and mumps vaccines derived from chicken cells: investigation of transmission to vaccine recipients:
Reverse transcriptase (RT) activity has been detected recently in all chicken cell-derived measles and mumps vaccines. A study of a vaccine manufactured in Europe indicated that the RT is associated with particles containing endogenous avian retrovirus (EAV-0) RNA and originates from the chicken embryonic fibroblasts (CEF) used as a substrate for propagation of the vaccine. We investigated the origin of RT in measles and mumps vaccines from a U.S. manufacturer and confirm the presence of RT and EAV RNA. Additionally, we provide new evidence for the presence of avian leukosis virus (ALV) in both CEF supernatants and vaccines. [87]
In Viral Nucleic Acids in Live-Attenuated Vaccines: Detection of Minority Variants and an Adventitious Virus, the process is admitted, yet rather downplayed in its extent, where viral material within a vaccine can recombine and turn pathogenic:
In very rare instances, one attenuated viral vaccine, the oral poliovirus vaccine (OPV), can accumulate mutations as well as recombine with other coinfecting enteroviruses and revert to a pathogenic state. (18, 24). Attenuated live vaccines also carry a potential risk of contamination with adventitious viruses introduced during the attenuation process, from the cell lines used, and/or from the animal sera or other biologics often used in cell cultures. Very early Theiler’s yellow fever attenuated virus was once “stabilized” with human plasma thought to contain hepatitis B virus, resulting in many cases of hepatitis (5, 28). Some early Sabin poliovirus vaccines were contaminated with the simian virus 40 (SV40) polyomavirus from the monkey cells used to amplify polioviruses. [88]
The Division of Viral Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drugs Administration (FDA), admitted in a publication, Issues associated with residual cell-substrate DNA in viral vaccines, that the contamination with viral substrates of commercial lots of vaccines was inevitable, as well as being potential carcinogens:
The presence of some residual cellular DNA derived from the production-cell substrate in viral vaccines is inevitable. Whether this DNA represents a safety concern, particularly if the cell substrate is derived from a tumor or is tumorigenic, is unknown. DNA has two biological activities that need to be considered. First, DNA can be oncogenic; second, DNA can be infectious. As part of our studies to assess the risk of residual cell-substrate DNA in viral vaccines, we have established assays that can quantify the biological activities of DNA. From data obtained using these assays, we have estimated the risk of an oncogenic or an infectious event from DNA. [89]
II. Immune Tolerance, HLA Variation, Disease Transmission and Outcome
Fast-forwarding to the present day, there has been a sudden change in some of the public opinion of those who question the narrative and recklessly jump to the conclusion that there are no such things as transmissible germs and viruses, at the suggestion of Thomas S. Cowan and his book, the Contagion Myth, who claims that germs and viruses cannot be transmitted, that all problems are toxic chemicals in nature, the underlying tone is that we live in harmony with germs and viruses. [90] Are we currently living in harmony with nature? Not at all, so why wouldn’t these viruses and microbes turn against us, with such widespread engineering and introduction of foreign biological constructs that the planet has never seen before? [91]
The germ denial discussion would polarize the two sides in typical fashion, making an already divided discussion polarized and more complicated. It pops up almost overnight in the middle of the COVID-19 situation after one of his videos went viral and received millions of views. It appears a convincing argument, since both Koch’s postulates and Rivers’ postulates do not satisfy the situation, and this remains with many other forms of infectious disease. However, Traub’s discovery in LCM and his later creation of widespread weapons and some natural diseases with a slow, debilitating nature, no outward symptoms and hard-to-isolate viruses and microbes that took to tissue and brain matter, obliterated both Koch’s and Rivers’ postulates, because the slow-virus disease, also seen in bacterial and fungal infections, basically, anything containing the immunosuppressive lipoproteins would cause a very different picture of disease, but nonetheless equally painful and misery-inducing, producing chronic disease and mental illness simultaneously, that was extremely difficult to diagnose and treat.
It would be hard to prove something caused the same disease in every subject, when the HLA-makeup of each person is variable, producing a variable response, most (roughly 85%) getting a disease that takes years to incubate and really gain momentum, while others may have an acute response (the much smaller minority of roughly 15%), [92] just as some people have aggressive hyperallergic reactions to vaccines, while some get a pronounced immunosuppression. Some may not get either forms, and that is the nature of the variable immune systems different people have. Not all people have the same immune system, and germs will produce a different picture in different people, so there is no unanimous result which these postulates can be satisfied.
There were some viruses, such as Newcastle Disease Virus and various retroviruses, that undressed their virions into small exosome-like particles, some have termed these viromicrosomes, [93] and the undressing occurs right before entering the cell, then hijacks parts of the cell lipids, before exiting as a complete virion, now containing pieces of the cell’s genetic material. [94] This would produce endless variants as the virus passed through any population with a variation of genes. [95] This result is typical with any virus or agent that contains these certain antigens and lipoproteins called fusion proteins. [96] The influenza groups, foot-and-mouth disease virus, HIV, and many additional pathogens contained such components.
The problem, however, is that the medical and science establishments of the time decided to bury Traub’s findings, first, because there was a deeper biological weapons context to all of this. Secondly, and perhaps more so, the discovery was also showing that the mechanisms of immune tolerance were quite similar to how western vaccination was playing out, being that there was indeed harm being done, a rebound effect in which the immune systems were being slowly burned out not to respond, but the harm was in some ways more extensive, proliferative, and permanent. [97] [98] [99] [100] The immune system not only fights off foreign invaders, but keeps us vital and vigorous to live life. Without this, one will have the full spectrum of chronic fatigue, fibromyalgia, meningo-encephalitis, and of course, mental illness. This is still, very much a disease, but can take some time to develop. This was discussed in two prior articles I’ve written. Tainted Immunity: Post-Vaccinal Encephalitis and the Chronic Plague of Societal Degeneration and Medical Misanthropology: A Tale of Vaccination, Clinical Psychiatry, and Mental Illness.
Cowan put forward the argument that the Spanish Flu was not transmissible, because Pfiffer’s bacillus isolated from cases of Spanish Flu used in experiments did not cause Spanish Flu in other subjects. [101] Though bacterial agents of many various kinds were isolated in brain and tissue samples of fatalities resulting from the epidemic, [102] the cause was viral in origin, [103] but of course, the effect of this virus on the immune system in the initial viral infection would cause a viral-bacterial synergy resulting in bronchopneumonia, which was a combined secondary infection, back in those days this was also called infectious respiratory catarrh, or ”mixed infections” another important line of work that Erich Traub studied in more depth. [104] [105] This was a process in which the virus came through and obliterated the immune system and the bacterial meningitis would often deliver the deathblow. [106] This is the nature of targeting and modulating the immune system, [107] throwing the immune system out of whack would open the flood gates for reactivation of latent germs and the invitation of secondary opportunistics, such as those seen in AIDS, but in a much more accelerated manner. It was not the result of Pfiffer’s Bacillus, and attempts to reproduce the disease with such a germ would typically be fruitless. This was just one example of some of the mistakes I noted reading Cowan’s book, he did not take into account many of these factors I am laying out now. In light of the slow-virus disease and variable HLA-makeup of different people, Cowan’s theories should be reconsidered and seen through the light of immune tolerance and HLA variation.
At any rate, it can be agreed that there are serious problems in the realm of vaccination having serious detrimental effects in public health amidst these immune complexes. [108] There are so many issues and complications involved within the inner mechanics of vaccination, especially in populations riddled with varying degrees of immunodeficiency. Vaccines may quiet the acute expression of disease by inducing tolerance to specific pathogens and viruses, which would be a good thing if not for the horrific rebound effect of causing severe long-term permanent chronic diseases. [109] [110] One can think of disease not just as an acute expression, but the other end of this spectrum is disease of a chronic nature that accompanies immunosuppression. [111]
The process is one in which the person contracts an infectious disease, say a virus or spirochetal infection from a tick bite, the onset of septicemia occurs, and this would present with a flu-like illness. This septicemic reaction then disables the immune system, [112] and while the immune system reaches a compromised state, latent herpesviruses like Epstein-Barr Virus (EBV), Human Herpesvirus-6 (HHV-6), Herpes-simplex (HSV-1), and many others, reactivate from within the B-cells, causing B-cell Immortalization, where unhealthy cells are in a sense zombified yet transformed into a veritable virus factory following the reactivation. [113] In normal subjects, these infected cells would normally undergo a process called apoptosis, where the unhealthy cell destroys itself so the immune system can then produce new healthy B-cells. [114] In this case, however, the B-cell Immortalization causes inhibition of apoptosis, [115] and the transformed, these zombified B-cell lives on indefinitely in a state of incompetence. [116]
The viruses that reactivate in this state of immunodeficiency may be numerous. The Epstein-Barr Virus (EBV) may be just one among many concurrent and persistent viral infections of the herpesvirus family among other latent vaccine viruses that come in with the multiple vaccines given during the lifetime of the individual. [117] Following this state of immunodeficiency, opportunistic infections will often present concurrent infections like Mycoplasma pneumoniae, Chlamydia pneumoniae, and many other pathogens that normally are not a problem for healthy individuals. [118] Occasionally, animal diseases not known to infect humans can be present which most doctors and even infectious disease specialists will have no experience in dealing with, such as granulencephalitis (Encephalitizoon caniculi), a blood parasite of rabbits. [119]
The secondary effect of the immune tolerant state is one of neurotropic effects on the brain and central nervous system. The neuroimmune system has to work overtime to keep up with the infectious invasion of para-infectious material like antigen, virus, and pathogenic microbes. Neurotropism is the degradation of the central nervous system and brain, and the result will impart neurological and psychological manifestations due to the continuous low-level neuroinflammation that results. [120] I covered the para-infectious nature of neurotropism and its effects in Medical Misanthropology: A Tale of Vaccination, Mental Illness, and Clinical Psychiatry, an article which cites many papers illustrating the nature of these processes on the brain and central nervous system. antigen alone will have the same neurotropic effect, invading the brain leading to chronic neuroinflammation and neurologic disease. [121] [122]
III. Viral Proliferation, Immune Tolerance, and Resulting Mental Illness in Targeted Nations of Bioterrorism & Over-Vaccination
If one studied the life work and publications of Erich Traub, this picture mirrors much of what Traub discussed in his published work, and the picture would present a very risky, dangerous road we’re going down. The massive rise in chronic disease, mental illness, and neurological disorders reflects the effect of both a collectively, overburdened immune system of the population, and, the unrestricted contamination of commercial vaccines, with many of the contaminant viruses being neurotropic, [123] the antigens and viral envelopes have an affinity for brain tissue and the nerves, [124] and the reactivation of latent herpesviruses, along with new viruses passed in through immunizations, harbors the conditions for such to occur. [125] This results in deterioration of the brain and central nervous system, resulting in neurological problems, and progressive degenerative diseases. [126] The autistic spectrum would also fall into this category. Extensive mental health problems would be expected.
Traub’s work with Borna Disease Virus, Eastern Equine Encephalitis, Pseudorabies, swine encephalomyelitis, neurotropic-modified Foot-and-Mouth Disease Virus (FMD), among other disease agents, gave him a superior understanding of the complex interrelationships between immune tolerance and neurotropism. In human beings, some of these same neurotropic viral infections have been documented and studied, and present with neurological, cognitive, and mental health problems. [127] The autistic spectrum of disease becomes relevant here, as a form of neurotropism which is many times accompanied by immune deficiencies, allergies, auto-immune problems, and so on. [128] This would lend more weight to the relevance of Traub’s work in these areas, [129] which brings in crucial elements relevant to biodefense and National Security, because a very serious health risk is present as several stealth pathogens are filtering through the population, without signs of slowing down, and the stacking of additional vaccines on top of those infected makes the problem infinitely more complex and problematic. [130] [131]
Vaccine revertants such as those described by Auwaerter et al., along with the reactivated herpesviruses are generally of the neurotropic class, and highly variable. [132] The action of systemic viral infections with a predilection for brain and nerve tissue has a profound effect on psychological process. Mental illness would be the inevitable expression of these viral infections and antigen, as German researcher Karl Bechter pointed out in his 2013 paper, Virus Infection as a Cause of Inflammation in Psychiatric Disorders:
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 sub-group of severe psychiatric disorders. [133]
Bechter also studied this further with one of Traub’s later colleagues, Rudolf Rott, published MRI in psychiatric patients with serum antibodies against Borna disease virus regarding the findings of Borna Disease Virus antibodies in psychiatric patients, as evidence of infection among the mentally ill, but not in the healthy controls:
Investigations in the FRG and the USA revealed the presence of serum antibodies against the [Borna Disease (BD)] virus in psychiatric patients with affective psychoses, but not in healthy controls. We demonstrated the occurrence of BD virus-specific antibodies in sera of about 7% of the psychiatric inpatients at our hospital, not only in patients with affective psychoses but also in those with other psychiatric disorders. By comparison, in surgical patients from an endemic region, only 3% were found to be seropositive, some of whom had psychiatric or neurological disturbances. The question was whether the BD virus-positive seroreaction was a coincidental and harmless finding or whether it could represent the cause of psychiatric disorders. [134]
Theoretically, a strike with several biological agents on a population for strategic purposes as a long-term strategy could realistically be carried out whereby a nation is systematically destroyed very slowly, starting from a few small incidents or maneuvers, (i.e. attacks that release infected arthropods into the ecosystem, contamination of commercial vaccines, gene therapies, and prophylactics), [135] the target nation would be largely unaware that it was even under attack, and if they began to catch on, it would seem smaller in scope, yet infinitely worse in actuality. [136] Its effects would be cumulative and gain momentum over many decades, with a culminating snowball effect restricting the response to the point of being overwhelmed and too heavily burdened by it to recuperate, [137] and for that reason it becomes a subject most relevant to Western & American National Security. Part of such an attack depends on the target country’s response, namely the deployment of vaccines, which make the agents released more vicious, as mentioned in The Darker Bioweapons Future, an intelligence assessment on biological warfare and bioterrorism:
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. [138]
IV. A Theoretical Picture of Systemic Immune Tolerance and Neurotropic Injury in Societal Structures
Because the immune tolerant condition tends to happen in varying degrees, usually simultaneously to auto-immune problems, [139] oftentimes subclinical or inapparent in outward appearance, [140] and since the condition of Traub’s immune tolerance was not given significant enough attention in public health’s attack on human infectious disease even after his publishing on it all the way up to his death in 1985, [141] a continual failure to detect chronic infections would inevitably result. Traub noted the lack of antibody response in tolerant carriers, which were also chronically infected and later displayed signs of chronic health problems, the picture of such an immunological burden in a society would, in theory, present very similarly to the conditions we are seeing today, which Traub first modeled in white mice:
Mice infected in utero with LCM virus carry large amounts of active virus in their blood and organs for many months and discharge considerable quantities of the agent with their secretions and excretions (11). This observation indicates continuous multiplication of the virus in the organs of such animals, which look like normal individuals in spite of their chronic infection. Intrauterine infection leads to a stable equilibrium between virus and body. It was also observed that mice infected in utero would develop practically no specific antibodies, while the sera of mature mice infected experimentally or by contact at least gave positive complement-fixation (CF) tests (9, 14).
Attempts to demonstrate neutralizing antibodies in the sera of such animals using customary techniques gave essentially negative results (for references see 13). More sensitive methods, however, have made the demonstration of such antibodies possible (7), Recent experiments have shown that their titer is relatively low and their antiviral action exceptionally slow (13). The failure to recognize this fact no doubt accounts for the negative results obtained earlier by different investigators. For several reasons it is still doubtful whether these antibodies represent the immunity factor of prime importance in mice recovered from experimental infection (10, 7, 13). The solid immunity of mice infected in utero is obviously not due to antibodies, since none could be demonstrated with sensitive methods even after repeated inoculations of virus (12, 13) and since life-long persistence of large amounts of active virus in the body would hardly be compatible with the antibody theory. [142]
Later in the same paper, Traub talked about the mechanisms of immune tolerance found in other antigens like pneumococcal polysaccharides:
The organs of congenitally infected mice, young or old, generally contained more antigen than those of mature mice infected artificially. The very high antigen content of the lymphatic system in tolerant animals has been correlated with the tolerance phenomenon and the possibility considered that their immunological apparatus may be blocked by specific antigen as in mice showing "immunological paralysis" following inoculation with large doses of pneumococcal polysaccharide. [143]
The academic and biodefense specialists have known about the mechanisms of immune tolerance in other areas. For instance, immune tolerance has gone by other names, such as endotoxin tolerance, [144] and, as Traub pointed out, immune paralysis which is perhaps a more fitting term. [145] With early studies supported by the National Institute of Allergy and Infectious Disease (NIAID), this is not a case where the science of immune tolerance was unknown and seen as a harmless or even healthy, it was deliberately settled on as a form of immunity, to allow vaccine practices and monopolies on public health operating under an outdated and incomplete picture of immunology to take precedence over well-being. Profiteering and selfish corporate agendas certainly come into play, giving them a reason to bury what Traub had contributed to immunology, in the public health system and medicine, by awarding the discovery to Burnet and Medawar regarding organ transplants. [146] The result would be chronic disease paralyzing the immune system like those who survive sepsis. [147]
One of Traub’s protégés in Germany, Zvonimir Dinter, writing in a later article submitted to the German medical journal Berliner und Münchener tierärztliche Wochenschrift in 1984, told his experience working with Traub, and suggested that he should have been part of the Nobel Prize for his discovery of immune tolerance in LCM virus:
Traub, "who started the whole thing." The TRAUB's lived on Riems in a mansion when I entered the villa, it was already twilight, you could hear the monotonous splashing of the Baltic Sea, it was a mood where memories are easily awakened. After coffee with cake, TRAUB told me how he came to the US when RICHARD E. SHOPE, the famous virologist from the Rockefeller Institute, spent his time in Giessen, among other places, in the early 1930s. Zwick's work on the Borna Disease attracted researchers who poured in... like TRAUB, who was already considered a student proficient in English, to SHOPE he was assigned as a language facilitator. SHOPE soon saw TRAUB's interest and talent in viral research and invited him to the Rockefeller Institute. Shope was right in his assumption. Much later (1959), he told me himself.
TRAUB's talent soon starts after he began research at Princeton, the Rockefeller Institute branch. The topic to which he dedicated his work in the first place was the behavior of the mouse lymphocytic choriomeningitis virus. A number of communications that began in Science and continued in the Journal of Experimental Medicine, and which are generally regarded as classical today, since "... many pioneering series of investigations in many of the key biological properties of the virus were established. "(1) When BURNET and MEDAWAR received the Nobel Prize in 1960 for their seminal immunological work, I, as a veterinarian and TRAUB’s employee, would have liked to see that he, too, had participated in the prize because what TRAUB already described in 1936 and 1939, was the mode of origin of the condition, which was later baptized with "immune tolerance" and which represented a pillar of Burnet's clone-selective theory (2). The American researcher HOTCHIN has appreciated TRAUB's dedication by giving him his monograph with the words: "To ERIC TRAUB who started the whole thing" (3). [148]
The condition and its process would also be increasingly more complex as vaccinations were stacked on top of those already dealing with one or several chronic viral infections congenitally transmitted from mother to newborn, with no outward signs of disease upon birth, tolerized to virus, yet the effect of infection in the lifetime of that individual would be cumulative, [149] with early and late onset disease, [150] while the increasing number of vaccines given in the schedule adds infinitely more burden to an already confused and exhausted immune system, [151] it is akin to trying to put a fire out with gasoline. Many people today can think of several families with autistic or mentally ill children, and the effect on a nation, if such angles were used in special weapons of bioterrorism geared for strategic, long-term attacks, a target country would be plagued by chronic health problems and mental illness, with failure to detect infection, and simply labelled ‘somatoform’ or ‘mentally ill’ with no infectious disease, [152] yet was very likely dealing with one or several infections. The course of disease by the immune tolerance complex would present only general similarities between subjects, with different courses and outcomes for each. [153] The result could be so various that the condition is grouped into many separate conditions between physical and mental health, leaving health practitioners and public health systems little to no understanding of the causal factors of immune tolerance and neurotropism.
The effect on mental health would present with varying degrees and combinations of neurotropism and damage to the brain, [154] expressing mood swings, lack of organization and cognitive abilities, irritability, rage, senseless acts of violence, irrational behaviors, lowered inhibitions resulting in an increase in criminal activity or deranged behavior, such that is very common in the headlines of Western nations today. [155] Simply put, to target the brain of a population would affect the societal structure as a whole, because the chaos of one effects the many, and when large numbers of unstable citizens with unpredictable and irrational or violent behaviors from neurotropic infections of the brain and CNS are scattered throughout its society presenting in this manner, [156] that is, infections passing congenitally through generations gaining more momentum in the subsequent generations infected, [157] the implications are systemic and far-reaching, tearing at the fabric of the society itself, as we are seeing the effects today, with Western countries leading in chronic disease and mental illnesses. [158] [159]
If this idea on the current picture of public health is taken as a whole, perhaps just as devastating effects would be felt by even the upper echelons of society, particularly in the science and medical communities, as the incompetence to deal with this problem inevitably reached its conclusion, [160] and the truth made its way out. [161] Perhaps the fact of the matter may be that the scientists and public health systems have no definitive game plan since treating virus infections is not curative but supportive. The integrity of the medical and scientific establishments in countries where the problem was consistently denied, covered-up, ignored, missed, or left unaddressed, would have its reputation greatly challenged in the public eye of trust. If specialists, along with pharmaceutical firms sought to influence the public health system’s officials and academic scientists in attempts to avoid dealing with this problem for profit-driven agendas, such as testing methods that miss the problem in very clever ways as to conceal the presence of infections and the immune tolerant state, there would have to be prosecutions, penalties, and reparations paid to those affected if trust were to be re-established. [162] Laws have been pushed in place which allow the drug firms, unprecedented control through experimental conditions on a public without its knowledge of experimental phases. [163]
Lyme disease and SARS-CoV-2 serve as modern examples of the corrupt practices in effect today, where science and public health officials are perpetuating the same fraud overlapping other diseases. [164] For example, the diagnostic approach to Lyme disease at the 1994 Dearborn conference attempted to phase out and scrub the seronegative infections in immune tolerant outcomes from the books, changing the definition of the disease to be only an acute presentation with a more robust immune response. [165] [166] This outcome would only present in a small minority of cases, while the rest would be immunosuppressed and overrun by chronic health problems, brushed under the rug and slandered as psychiatric cases. [167] [168]
The LYMErix vaccine would also induce the immune tolerant state and injuries would follow. [169] Indeed, the vaccine had to be pulled from the market within two years of its implementation when reports of severe adverse events began to surface, [170] but the public health officials attempted to coverup the problem by having the doctors label the reactions unrelated to the vaccine. [171] Finally, an FDA hearing led to its ultimate removal from the market, with disturbing testimonies from those who had now permanent health problems and unable to work or live the active life they once had. [172]
SARS-CoV-2 is another example of the same class of antigen on a virus disease. [173] This problem spells out very clearly the problematic nature of public health’s reliance on antibody response and acute expression. [174] The immune tolerance would be achieved in the first two weeks of infection, with the end result of reaching an indefinite state of immune tolerance. [175] They began to employ semantical terms like “COVID long-haulers,” and “long-COVID,” to mask the idea of chronic infection. [176] This post-viral syndrome described was the same as that described in other immune tolerant states following infection, such as post-polio syndrome, [177] post-Ebola syndrome, [178] post-treatment Lyme disease, [179] and post- anything was a term for the immune tolerance imparted from the initial infection, as Kathleen Dickson of the TruthCures organization accurately described this as a post-sepsis syndrome. [180]
The SARS-CoV-2 vaccines would also be inducing immune tolerance as its mechanism for immunity, with lipids polyethylene glycol (PEG) and other synthetic chemicals to mimic the lipid envelope expressed on the virus. [181] PEG is known to cause immune tolerance, [182] and this would indicate that the mechanism for immunity they were aiming for was immune tolerance, or burning out the immune system. [183] This same mechanism of immune tolerance was also decided as an acceptable form of immunity in the poultry industry after widespread epidemics in the 1950s. [184] [185] They considered burning out the immune system a viable solution to infectious disease, [186] and this same approach carried over into the approach to public health in humans. [187] In effect, they were adding insult to injury with more severe and permanent degrees of immunosuppression and tolerance to mask the acute diseases, which they considered the only form of disease, while labelling the chronic cases a social phenomenon or construct of somatoform. [188]
Had Traub’s discovery of the para-infectious role of immunological tolerance been accepted and included into the science back in the early 1960s, [189] public health and medicine would look very different today. [190] The entire spectrum of disease and immunology would have been reconfigured to be aligned with truth and legitimate science, which could have put forward legitimate solutions and remove the unsound and destructive health effects of vaccination. [191] [192] Instead, the entire spectrum of chronic disease was purposefully buried and denied, [193] [194] in opposition to legitimate science. [195] Profiteering took precedence over genuine well-being, [196] monopoly on health practices and experimental testing programs would be safeguarded by laws passed to protect Big Pharma under the pretext of biodefense, [197] allowing the people of the country vulnerable and lied to. [198] The science was not working in the aims of Greater Good, but a greater greed with an insatiable appetite for power and control, [199] as the chronic health problems and secondary neurotropism set the pretext in which the implosion of Western society would inevitably result. [200] [201]
In the words of Dr. Erich Traub’s protégé, Werner Schafer, a telling revelation spoken at a conference for the Office of Naval Research in Kansas in 1962 may once again hold the key to understanding the situation, albeit through the overtones of unbelievable irony:
I hope I have been able to demonstrate that the concentrated action of our group on a very small sector of animal virology was not quite unsuccessful but has created at least some ideas of possibly a more general importance for the fight against virus diseases. At the present time, when concentrated scientific activity is often directed toward the destruction and not toward the preservation of life, one might fear that the phrase "concentration is the prudence of life" will someday be inverted into "concentration is the stupidity of life." To avoid such an occurrence, scientific workers all over the world would do well to return to the ethics of the stoicist Seneca, who noted in his Naturales Quaestiones that "by exploration of the facts natural sciences base the moral life of man on a solid foundation; they liberate him from fear and let him recognize the glory and magnitude of divine creation."
- Dr. Werner Schäfer, ONR lecture, presented at the Annual Meeting of the American Society for Microbiology, Kansas City, Mo., 6 May 1962. [202]
Endnotes/References
[1] 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
[2] Dinter, Z. Persönaliches, Begegnungen mit Erich Traub.[Personal Encounters with Erich Traub] Berl. Munch. Tier. Woch. 96. 70-72. (1984)
[3] with the para-infectious origins of immune tolerance obscured and attributed to organ transplants only, the entire spectrum of chronic disease would be buried, and one-half of the spectrum of immunology would be ignored. The science and public health would keep antibody response and acute presentation of disease the only form of disease, and this was erroneous, incomplete, and unscientific.
[4] Lyme disease being one example. See: Dickson, Kathleen. TRUTHCURES.ORG CRIMINAL CHARGE SHEETS JUNE 2017, 2017, pp. 39. https://docs.wixstatic.com/ugd/47b066_01d68b1309ae457b81df1e06e6beae1e.pdf
[5] See the mechanisms described in Traub’s first paper: Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).
[6] Schmidt RE, Grimbacher B, Witte T. Autoimmunity and primary immunodeficiency: two sides of the same coin? Nat Rev Rheumatol. 2017 Dec 19;14(1):7-18. doi: 10.1038/nrrheum.2017.198. PMID: 29255211.
[7] Pierangeli A, Antonelli G, Gentile G. Immunodeficiency-associated viral oncogenesis. Clin Microbiol Infect. 2015 Nov;21(11):975-83. doi: 10.1016/j.cmi.2015.07.009. Epub 2015 Jul 18. PMID: 26197213.
[8] Lomonte P. Herpesvirus Latency: On the Importance of Positioning Oneself. Adv Anat Embryol Cell Biol. 2017;223:95-117. doi: 10.1007/978-3-319-53168-7_5. PMID: 28528441.
[9] Kerr JR. Epstein-Barr virus (EBV) reactivation and therapeutic inhibitors. J Clin Pathol. 2019 Oct;72(10):651-658. doi: 10.1136/jclinpath-2019-205822. Epub 2019 Jul 17. PMID: 31315893.
[10] Di Lorenzo, Antonino et al. “Toll-Like Receptor 2 at the Crossroad between Cancer Cells, the Immune System, and the Microbiota.” International journal of molecular sciences vol. 21,24 9418. 10 Dec. 2020, doi:10.3390/ijms21249418
[11] Mottahedin A, Svedin P, Nair S, Mohn CJ, Wang X, Hagberg H, Ek J, Mallard C. Systemic activation of Toll-like receptor 2 suppresses mitochondrial respiration and exacerbates hypoxic-ischemic injury in the developing brain. J Cereb Blood Flow Metab. 2017 Apr;37(4):1192-1198. doi: 10.1177/0271678X17691292. Epub 2017 Jan 1. PMID: 28139935; PMCID: PMC5453473.
[12] 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).
[13] Traub, E. & K. Beller. Untersuchungen uber die ansteckende Blutarmut der Pferde. Immunitatsversuche. [Immunization experiments in equine infectious anaemia]. Monatshefte fur Praktische Tierheilkunde; 3:193-206. (1942, 1951). [translated to English by A. Finnegan 2019]
[14] One excellent example of this is the research put together by Miss Kathleen Dickson, through her organization, Truthcures, and especially the YouTube video, Lyme Cryme, seen here: https://www.youtube.com/watch?v=f8DU1Z6R-ms&t=692s
[15] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).
[16] Shope, R. E. (1935). Experiments on The Epidemiology Of Pseudorabies: I. Mode Of Transmission Of The Disease In Swine And Their Possible Role In Its Spread To Cattle. Journal of Experimental Medicine, 62(1), 85-99. doi:10.1084/jem.62.1.85
[17] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).
[18] Corner, G. W. (1965). A history of the Rockefeller Institute: 1901-1953: Origins and growth. New York: The Rockefeller Institute Press., pp. 408-409
[19] 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).
[20] 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).
[21] 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]
[22] 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
[23] 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)
[24] Hotchin, John. 1971. Monographs in Virology: Persistent and Slow Virus Infections. Karger.
[25] 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).
[26] 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]
[27] Traub, E. Can LCM virus cause lymphomatosis in mice? Archiv Fur Die Gesamte Virusforschung, 11(5), 667-682. doi:10.1007/bf01243307. (1962).
[28] Traub, E. Choriomenigitis der Mäuse. Handbuch der Viruskrankheiten, (E. Gildenmeister, E. Haagen & O. Waldmann, eds). Fischer-Verlag, Jena, Vol. 2, Ch. 7. 355-364. (1939). [Translated to English by A. Finnegan (2019)]
[29] 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).
[30] Lyme disease being a good example, see: Dickson, K. “CRIMINAL CHARGE SHEETS JUNE 2017 Lobbying for a Hearing for Referral to the USDOJ for a Prosecution of the Lyme Disease Crimes.” 2017. Published at: https://docs.wixstatic.com/ugd/47b066_01d68b1309ae457b81df1e06e6beae1e.pdf
[31] This is observable in the relation to chronic neurologic outcomes of vaccine adverse events: Marks, Donald H. ‘Neurological Complications of Vaccination with Outer Surface Protein A (OspA)’. 1 Jan. 2011 : 89 – 96.
[32] Sejvar, James. "Vaccines and Neurologic Disease." Seminars in Neurology 31, no. 03 (2011): 338-55. doi:10.1055/s-0031-1287655.
[33] 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).
[34] Cherkasova, Elena A., Ekaterina A. Korotkova, Maria L. Yakovenko, Olga E. Ivanova, Tatyana P. Eremeeva, Konstantin M. Chumakov, and Vadim I. Agol. 2002. “Long-Term Circulation of Vaccine-Derived Poliovirus That Causes Paralytic Disease.” Journal of Virology 76 (13): 6791–99. https://doi.org/10.1128/jvi.76.13.6791-6799.2002.
[35] Cassisi, G, P Sarzi-Puttini, and M Cazzola. 2011. “Chronic Widespread Pain and Fibromyalgia: Could There Be Some Relationships with Infections and Vaccinations?” Clinical and Experimental Rheumatology. U.S. National Library of Medicine. 2011. https://www.ncbi.nlm.nih.gov/pubmed/22243559.
[36] Cherkasova, E. A., et al. “Spread of Vaccine-Derived Poliovirus from a Paralytic Case in an Immunodeficient Child: an Insight into the Natural Evolution of Oral Polio Vaccine.” Journal of Virology, vol. 79, no. 2, 2004, pp. 1062–1070., doi:10.1128/jvi.79.2.1062-1070.2005.
[37] Croft, P. B. (1969). Para-infectious and post-vaccinal encephalomyelitis. Postgraduate Medical Journal, 45(524), 392–400. doi:10.1136/pgmj.45.524.392
[38] 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
[39] Abu-Akkada SS, El Kerdany ED, Mady RF, Diab RG, Khedr GA, Ashmawy KI, Lotfy WM. Encephalitozoon cuniculi infection among immunocompromised and immunocompetent humans in Egypt. Iran J Parasitol. 2015 Oct-Dec;10(4):561-70. PMID: 26811722; PMCID: PMC4724832.
[40] Duintjer Tebbens RJ, Thompson KM. Comprehensive screening for immunodeficiency-associated vaccine-derived poliovirus: an essential oral poliovirus vaccine cessation risk management strategy. Epidemiol Infect. 2017 Jan;145(2):217-226. doi: 10.1017/S0950268816002302. Epub 2016 Oct 20. PMID: 27760579; PMCID: PMC5197684
[41] see: Dickson, K. “CRIMINAL CHARGE SHEETS JUNE 2017 Lobbying for a Hearing for Referral to the USDOJ for a Prosecution of the Lyme Disease Crimes.” 2017. Published at: https://docs.wixstatic.com/ugd/47b066_01d68b1309ae457b81df1e06e6beae1e.pdf
[42] Shah, Keerti, and Neal Nathanson. “Human Exposure To Sv40: Review And Comment.” American Journal of Epidemiology, vol. 103, no. 1, 1976, pp. 1–12., doi:10.1093/oxfordjournals.aje.a112197 Retrieved from https://academic.oup.com/aje/article-abstract/103/1/1/151919?redirectedFrom=fulltext, or: https://www.scribd.com/document/409584571/Human-Exposure-to-SV40-Review-and-Comment-Carcinogens-in-Vaccines
[43] Baldwin, K. J., & Cummings, C. L. (2018). Herpesvirus Infections of the Nervous System. CONTINUUM: Lifelong Learning in Neurology, 24, 1349–1369. doi:10.1212/con.0000000000000661
[44] This is essentially the same mechanism in the human with the herpesvirus class, as the LCM virus in mice.
[45] Shah, Keerti, and Neal Nathanson. “Human Exposure To Sv40: Review And Comment.” American Journal of Epidemiology, vol. 103, no. 1, 1976, pp. 1–12., doi:10.1093/oxfordjournals.aje.a112197 Retrieved from https://academic.oup.com/aje/article-abstract/103/1/1/151919?redirectedFrom=fulltext, or: https://www.scribd.com/document/409584571/Human-Exposure-to-SV40-Review-and-Comment-Carcinogens-in-Vaccines
[46] Drăgănescu N, Gheorghiu V, Mihalache G. Encefalita postvaccinală la un sugar cu infecţie herpetică latentă [Post-vaccinal encephalitis in an infant with latent herpes infection]. Stud Cercet Inframicrobiol. 1970;21(5):385-9. Romanian. PMID: 4395307.
[47] Traub, E. A Filterable Virus Recovered from White Mice. Science, 81. (2099), 298-299. doi:10.1126/science.81.2099.298. (1935).
[48] Cassisi, G, P Sarzi-Puttini, and M Cazzola. 2011. “Chronic Widespread Pain and Fibromyalgia: Could There Be Some Relationships with Infections and Vaccinations?” Clinical and Experimental Rheumatology. U.S. National Library of Medicine. 2011. https://www.ncbi.nlm.nih.gov/pubmed/22243559
[49] A case in point: Valsamakis, A, P G Auwaerter, B K Rima, H Kaneshima, and D E Griffin. 1999. “Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue.” Journal of Virology. American Society for Microbiology. October 1999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC112900/
[50] Croft, P. B. (1969). Para-infectious and post-vaccinal encephalomyelitis. Postgraduate Medical Journal, 45(524), 392–400. doi:10.1136/pgmj.45.524.392
[51] “The Growing Crisis of Chronic Disease in the United States.” The Relief Work, 13 Jan. 2016, https://thereliefwork.com/2016/01/the-growing-crisis-of-chronic-disease-in-the-united-states/
[52] Hunter, Philip. “Is Political Correctness Damaging Science? Peer Pressure and Mainstream Thinking May Discourage Novelty and Innovation.” EMBO reports. U.S. National Library of Medicine, May 2005. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299305/
[53] Case in point: Valsamakis, A, P G Auwaerter, B K Rima, H Kaneshima, and D E Griffin. 1999. “Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue.” Journal of Virology. American Society for Microbiology. October 1999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC112900/
[54] Torisu, Hiroyuki, and Kenji Okada. “Vaccination-Associated Acute Disseminated Encephalomyelitis.” Vaccine, U.S. National Library of Medicine, 14 Feb. 2019, www.ncbi.nlm.nih.gov/pubmed/30683508
[55] Drăgănescu, N, et al. “Post-Vaccinal Encephalitis in an Infant with Latent Herpes Infection.” Studii Si Cercetari De Inframicrobiologie, U.S. National Library of Medicine, 1970, www.ncbi.nlm.nih.gov/pubmed/4395307
[56] 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).
[57] “The Growing Crisis of Chronic Disease in the United States.” The Relief Work, 13 Jan. 2016, https://thereliefwork.com/2016/01/the-growing-crisis-of-chronic-disease-in-the-united-states/
[58] Walton, Alice G. “Why More Americans Suffer From Mental Disorders Than Anyone Else.” The Atlantic, Atlantic Media Company, 3 Oct. 2011, www.theatlantic.com/health/archive/2011/10/why-more-americans-suffer-from-mental-disorders-than-anyone-else/246035/
[59] “Vaccination and Immunization Statistics.” UNICEF DATA, data.unicef.org/topic/child-health/immunization/
[60] Londoño, Diana, and Diego Cadavid. “Bacterial lipoproteins can disseminate from the periphery to inflame the brain.” The American journal of pathology vol. 176,6 (2010): 2848-57. doi:10.2353/ajpath.2010.091235
[61] Marks, D. H., “Neurological Complications of Vaccination with Outer Surface Protein A (OspA).” International Journal of Risk & Safety in Medicine. IOS Press. January 1, 2011. https://content.iospress.com/articles/international-journal-of-risk-and-safety-in-medicine/jrs527
[62] Sejvar, James. "Vaccines and Neurologic Disease." Seminars in Neurology 31, no. 03 (2011): 338-55. doi:10.1055/s-0031-1287655.
[63] Cassisi, G, P Sarzi-Puttini, and M Cazzola. 2011. “Chronic Widespread Pain and Fibromyalgia: Could There Be Some Relationships with Infections and Vaccinations?” Clinical and Experimental Rheumatology. U.S. National Library of Medicine. 2011. https://www.ncbi.nlm.nih.gov/pubmed/22243559
[64] Krueger, G. R. F., & Ramon, A. (1988). Overview of immunopathology of chronic active herpesvirus infection. Journal of Virological Methods, 21(1-4), 11–18. doi:10.1016/0166-0934(88)90048-1
[65] “Birth-18 Years Immunization Schedule | CDC.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html
[66] Cassisi, G, P Sarzi-Puttini, and M Cazzola. 2011. “Chronic Widespread Pain and Fibromyalgia: Could There Be Some Relationships with Infections and Vaccinations?” Clinical and Experimental Rheumatology. U.S. National Library of Medicine. 2011. https://www.ncbi.nlm.nih.gov/pubmed/22243559
[67] 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
[68] A case in point: Helaly, G. F., Elsheredy, A. G., El Basset Mousa, A. A., Ahmed, H. K. F., & Oluyemi, A. E.-G. S. (2016). Seronegative and occult hepatitis C virus infections in patients with hematological disorders. Archives of Virology, 162(1), 63–69. doi:10.1007/s00705-016-3049-7
[69] currently, children are expected to have around 15 vaccines, with up to 4 follow-up shots by the time they are 15 months old, which is extremely burdensome, when children that young don’t have fully developed immune systems yet, and many of them are already carrying a burden from RNA viruses transmitted to them congenitally by the mother. These same recipients are expected to have another 15 vaccines with several folowups, spanning to the time they reach adulthood. They are also recommended to have seasonal flu shots. If even one of these vaccines contain either Mycoplasma or viral contaminants, the damage could be extensive, permanent, and even deadly. For list and schedule, refer to: “Birth-18 Years Immunization Schedule | CDC.” n.d. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention. Accessed July 28, 2019. https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html
[70] Croft, P. B. “Para-Infectious and Post-Vaccinal Encephalomyelitis.” Postgraduate Medical Journal, vol. 45, no. 524, Jan. 1969, pp. 392–400., doi:10.1136/pgmj.45.524.392., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2466726/
[71] As discussed in: Office of Transnational Issues (OTI),”The Darker Bioweapons Future,” (Unclassified Intelligence Report). Directorate of Intelligence, Central Intelligence Agency (CIA). 3 December 2003. Retrieved from: https://www.cia.gov/library/readingroom/docs/DOC_0001298811.pdf
[72] “The Growing Crisis of Chronic Disease in the United States.” The Relief Work, 13 Jan. 2016, https://thereliefwork.com/2016/01/the-growing-crisis-of-chronic-disease-in-the-united-states/
[73] Siddique, Haroon. 2018. “Mental Health Disorders on Rise among Children.” The Guardian. Guardian News and Media. November 22, 2018. https://www.theguardian.com/society/2018/nov/22/mental-health-disorders-on-rise-among-children-nhs-figures
[74] Valsamakis, A, P G Auwaerter, B K Rima, H Kaneshima, and D E Griffin. 1999. “Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue.” Journal of Virology. American Society for Microbiology. October 1999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC112900/
[75] Traub, E. Uber Immunität und aktive Immunisierung gegen Viruskrankheiten [About Immunity and Active Immunization Against Viral Diseases.] Zeit. Infek. Krank. Hyg. Haus. Vol. 45 (1). 1-36. (1939). [Translated to English by A. Finnegan 2019]
[76] Baldwin, K. J., & Cummings, C. L. (2018). Herpesvirus Infections of the Nervous System. CONTINUUM: Lifelong Learning in Neurology, 24, 1349–1369. doi:10.1212/con.0000000000000661
[77] Sheng-Fowler, L., Lewis, A. M., & Peden, K. (2009). Issues associated with residual cell-substrate DNA in viral vaccines. Biologicals, 37(3), 190–195. doi:10.1016/j.biologicals.2009.02.015
[78] Croft, P. B. (1969). Para-infectious and post-vaccinal encephalomyelitis. Postgraduate Medical Journal, 45(524), 392–400. doi:10.1136/pgmj.45.524.392
[79] A case in point: Valsamakis, A, P G Auwaerter, B K Rima, H Kaneshima, and D E Griffin. 1999. “Altered Virulence of Vaccine Strains of Measles Virus after Prolonged Replication in Human Tissue.” Journal of Virology. American Society for Microbiology. October 1999. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC112900/
[80] Altamirano, Jonathan et al. “OPV Vaccination and Shedding Patterns in Mexican and US Children.” Clinical infectious diseases : an official publication of the Infectious Diseases Society of America vol. 67,suppl_1 (2018): S85-S89. doi:10.1093/cid/ciy636
[81] Sheng-Fowler, L., Lewis, A. M., & Peden, K. (2009). Issues associated with residual cell-substrate DNA in viral vaccines. Biologicals, 37(3), 190–195. doi:10.1016/j.biologicals.2009.02.015
[82] “PREVENTING ANOTHER SV40 TRAGEDY: ARE TODAY'S VACCINE SAFETY PROTOCOLS EFFECTIVE? : Committee on Government Reform.” 2003. Internet Archive. Government Publishing Office. November 13, 2003. https://archive.org/details/gov.gpo.fdsys.CHRG-108hhrg92772?q=SV40
[83] Shah, Keerti, and Neal Nathanson. “Human Exposure To Sv40: Review And Comment.” American Journal of Epidemiology, vol. 103, no. 1, 1976, pp. 1–12., doi:10.1093/oxfordjournals.aje.a112197 Retrieved from https://academic.oup.com/aje/article-abstract/103/1/1/151919?redirectedFrom=fulltext, or: https://www.scribd.com/document/409584571/Human-Exposure-to-SV40-Review-and-Comment-Carcinogens-in-Vaccines
[84] Ibid.
[85] Cutrone, Rochelle, et al. “Some Oral Poliovirus Vaccines Were Contaminated with Infectious SV40 after 1961.” Cancer Research, American Association for Cancer Research, 15 Nov. 2005, cancerres.aacrjournals.org/content/65/22/10273.article-info
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[89] Sheng-Fowler, L., Lewis, A. M., & Peden, K. (2009). Issues associated with residual cell-substrate DNA in viral vaccines. Biologicals, 37(3), 190–195. doi:10.1016/j.biologicals.2009.02.015
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[97] 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
[98] Cassisi, G, P Sarzi-Puttini, and M Cazzola. 2011. “Chronic Widespread Pain and Fibromyalgia: Could There Be Some Relationships with Infections and Vaccinations?” Clinical and Experimental Rheumatology. U.S. National Library of Medicine. 2011. https://www.ncbi.nlm.nih.gov/pubmed/22243559.
[99] Sejvar, James. "Vaccines and Neurologic Disease." Seminars in Neurology 31, no. 03 (2011): 338-55. doi:10.1055/s-0031-1287655.
[100] Croft, P. B. (1969). Para-infectious and post-vaccinal encephalomyelitis. Postgraduate Medical Journal, 45(524), 392–400. doi:10.1136/pgmj.45.524.392
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[109] see LYMErix Vaccine Victim Testimony to the FDA 2001: https://www.scribd.com/document/485041723/LYMErix-Vaccine-Victim-Testimony-to-the-FDA-2001
[110] Sejvar, James. "Vaccines and Neurologic Disease." Seminars in Neurology 31, no. 03 (2011): 338-55. doi:10.1055/s-0031-1287655.
[111] 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
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[120] Bechter, K. (2013). Virus Infection as a Cause of Inflammation in Psychiatric Disorders. Modern Trends in Pharmacopsychiatry, 49–60. doi:10.1159/000343967
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[130] “The Growing Crisis of Chronic Disease in the United States.” The Relief Work, 13 Jan. 2016, https://thereliefwork.com/2016/01/the-growing-crisis-of-chronic-disease-in-the-united-states/
[131] Siddique, Haroon. 2018. “Mental Health Disorders on Rise among Children.” The Guardian. Guardian News and Media. November 22, 2018. https://www.theguardian.com/society/2018/nov/22/mental-health-disorders-on-rise-among-children-nhs-figures
[132] Rubin, Steven A et al. “Changes in mumps virus gene sequence associated with variability in neurovirulent phenotype.” Journal of virology vol. 77,21 (2003): 11616-24. doi:10.1128/jvi.77.21.11616-11624.2003
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[137] reflecting that of LCM in mice, see: 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).
[138] Office of Transnational Issues (OTI),”The Darker Bioweapons Future,” (Unclassified Intelligence Report). Directorate of Intelligence, Central Intelligence Agency (CIA). 3 December 2003. Retrieved from: https://www.cia.gov/library/readingroom/docs/DOC_0001298811.pdf
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[140] 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).
[141] 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
[142] 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).
[143] Ibid.
[144] MULHOLLAND, J H et al. “QUANTITATIVE STUDIES OF FEBRILE TOLERANCE AND LEVELS OF SPECIFIC ANTIBODY EVOKED BY BACTERIAL ENDOTOXIN.” The Journal of clinical investigation vol. 44,6 (1965): 920-8. doi:10.1172/JCI105209
[145] Berger, F. M., & Fukui, G. M. (1963). Endotoxin Induced Resistance to Infections and Tolerance. Experimental Biology and Medicine, 114(3), 780–783. doi:10.3181/00379727-114-28796
[146] Silverstein, Arthur M. “The Curious Case of the 1960 Nobel Prize to Burnet and Medawar.” Immunology. John Wiley and Sons Inc., March 2016. https://www.ncbi.nlm.nih.gov/pubmed/26790994
[147] Arens, C et al. “Sepsis-induced long-term immune paralysis--results of a descriptive, explorative study.” Critical care (London, England) vol. 20 93. 29 Feb. 2016, doi:10.1186/s13054-016-1233-5
[148] Dinter, Z. Persönaliches, Begegnungen mit Erich Traub.[Personal Encounters with Erich Traub] Berl. Munch. Tier. Woch. 96. 70-72. (1984)
[149] Traub, E. . Observations on “Late onset disease” and Tumor Incidence in Different Strains of Laboratory Mice infected Congenitally with LCM Virus: II. Experiments with Inbred CBA/J mice. Zentralblatt Für Veterinärmedizin Reihe B, 22(9), 783-792. (1975, 2010) doi:10.1111/j.1439-0450.1975.tb00644.x.
[150] 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
[151] “Birth-18 Years Immunization Schedule | CDC.” n.d. Centers for Disease Control and Prevention. Centers for Disease Control and Prevention. Accessed July 28, 2019. https://www.cdc.gov/vaccines/schedules/hcp/imz/child-adolescent.html
[152] 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.
[153] This would be based on the assessment of genetic variability and predispositions or susceptibilities of each, the variability of pathogens accumulated, as well as secondary opportunistics, and the combinations therein are virtually endless.
[154] Brody, J. A., W. J. Hadlow, J. Hotchin, R. T. Johnson, H. Koprowski, and L. T. Kurland. “Soviet Search for Viruses That Cause Chronic Neurologic Diseases in the U.S.S.R.” Science 147, no. 3662 (May 1965): 1114–16. https://doi.org/10.1126/science.147.3662.1114
[155] Bechter, K. (2013). Virus Infection as a Cause of Inflammation in Psychiatric Disorders. Modern Trends in Pharmacopsychiatry, 49–60. doi:10.1159/000343967
[156] Siddique, Haroon. 2018. “Mental Health Disorders on Rise among Children.” The Guardian. Guardian News and Media. November 22, 2018. https://www.theguardian.com/society/2018/nov/22/mental-health-disorders-on-rise-among-children-nhs-figures
[157] as seen in Traub’s studies of mouse colonies: 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).
[158] Siddique, Haroon. 2018. “Mental Health Disorders on Rise among Children.” The Guardian. Guardian News and Media. November 22, 2018. https://www.theguardian.com/society/2018/nov/22/mental-health-disorders-on-rise-among-children-nhs-figures
[159] “The Growing Crisis of Chronic Disease in the United States.” The Relief Work, 13 Jan. 2016, https://thereliefwork.com/2016/01/the-growing-crisis-of-chronic-disease-in-the-united-states/
[160] Tim, Kae. “Goldman Sachs Asks in Biotech Research Report: 'Is Curing Patients a Sustainable Business Model?'.” CNBC, CNBC, 11 Apr. 2018, www.cnbc.com/2018/04/11/goldman-asks-is-curing-patients-a-sustainable-business-model.html
[161] Persing, David H. INFECTION, CANCER, AND THE IMMUNE RESPONSE. The Infectious Etiology of Chronic Diseases Defining the Relationship, Enhancing the Research, and Mitigating the Effects; Workshop Summary. National Acad. Press, 2004., pp. 154-173
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[163] “42 U.S. Code § 247d–7e - Biomedical Advanced Research and Development Authority.” Legal Information Institute, Legal Information Institute, www.law.cornell.edu/uscode/text/42/247d-7e
[164] i.e only focusing on the acute cases while denying the chronic outcomes and after-effects of the disabled immune system, or masking the problems with semantics. The vaccines were only working to induce tolerance, which only quieted the acute manifestations, and suppress clinical symptoms. Yet, the over-exhausted individual would experience a long-term chronic disease that was demoralizing and incapacitating.
[165] Proceedings of the Second National Conference on Serologic Diagnosis of Lyme Disease: October 27-29, 1994, Dearborn, Michigan. Washington, D.C.: Association, 1994.
[166] Dickson, K. “CRIMINAL CHARGE SHEETS JUNE 2017 Lobbying for a Hearing for Referral to the USDOJ for a Prosecution of the Lyme Disease Crimes.” 2017. Published at: https://docs.wixstatic.com/ugd/47b066_01d68b1309ae457b81df1e06e6beae1e.pdf
[167] Aronowitz, R A. “Lyme Disease: the Social Construction of a New Disease and Its Social Consequences.” The Milbank quarterly. U.S. National Library of Medicine, 1991. https://www.ncbi.nlm.nih.gov/pubmed/2034186
[168] 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
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[171] This can be realized from the testimony given to the FDA by those with adverse events, including in their testimony that doctors were telling the patients it wasn’t the vaccine causing the sudden onset of health problems, and even went as far as to persuade them to continue taking the subsequent shots, which made them much sicker and injuries more permanent. See FDA testimony on LYMErix vaccine victim testimony
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The Pfizer-BioNTech COVID-19 Vaccine is supplied as a frozen suspension in multiple dose vials; each vial must be diluted with 1.8 mL of sterile 0.9% Sodium Chloride Injection, USP prior to use to form the vaccine. Each dose of the Pfizer-BioNTech COVID-19 Vaccine contains 30 mcg of a nucleoside-modified messenger RNA (modRNA) encoding the viral spike (S) glycoprotein of SARS-CoV-2.
Each dose of the Pfizer-BioNTech COVID-19 Vaccine also includes the following ingredients: lipids (0.43 mg (4-hydroxybutyl)a zanediyl)bis( hexane-6 ,1-diyl)bis(2-hexyldecanoate), 0.05 mg 2[(polyethylene glycol)-2000]-N,N-ditetradecylacetamide, 0.09 mg 1,2-distearoyl-sn-glycero-3 -phosphocholine , and 0.2 mg cholesterol), 0.01 mg potassium chloride, 0.01 mg monobasic potassium phosphate, 0.36 mg sodium chloride, 0.07 mg dibasic sodium phosphate dihydrate, and 6 mg sucrose. The diluent (0.9% Sodium Chloride Injection, USP) contributes an additional 2.16 mg sodium chloride per dose.
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[190] For example, chronic disease would have been taken seriously, and profiteering at our expense would have been harder. As we stand right now, this is where we’re at, with Goldman-Sachs declaring there is no sustainable money-making in cures: Kae, Tim. “Goldman Sachs Asks in Biotech Research Report: 'Is Curing Patients a Sustainable Business Model?'.” CNBC, CNBC, 11 Apr. 2018, www.cnbc.com/2018/04/11/goldman-asks-is-curing-patients-a-sustainable-business-model.html
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[197] “42 U.S. Code § 247d–7e - Biomedical Advanced Research and Development Authority.” Legal Information Institute. Legal Information Institute, n.d. https://www.law.cornell.edu/uscode/text/42/247d-7e
[198] “50 U.S. Code § 1520a - Restrictions on Use of Human Subjects for Testing of Chemical or Biological Agents.” Legal Information Institute. Legal Information Institute, n.d. https://www.law.cornell.edu/uscode/text/50/1520a
This is nullified by:
“50 U.S. Code Chapter 33 - WAR POWERS RESOLUTION.” Legal Information Institute. Legal Information Institute, n.d. https://www.law.cornell.edu/uscode/text/50/chapter-33
“50 U.S. Code Chapter 34 - NATIONAL EMERGENCIES.” Legal Information Institute. Legal Information Institute, n.d. https://www.law.cornell.edu/uscode/text/50/chapter-34
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download the paper on Academia and share with as many people as possible as it may save lives: https://www.academia.edu/44865954/Immune_Tolerance_and_Slow_Virus_Disease_Skeletons_in_the_Closet_of_Western_Science_and_Public_Health
download the paper on Academia and share with as many people as possible as it may save lives: https://www.academia.edu/44865954/Immune_Tolerance_and_Slow_Virus_Disease_Skeletons_in_the_Closet_of_Western_Science_and_Public_Health