The Causes of Autism

July 24, 2026

Reading “The Wuhan Cover Up” by the current Secretary of HHS has provided context I did not realize would impact my current paper regarding the history of bioweapons research via the Operation Paperclips, the Geneva Protocol and BWC, the Patriot Act, and the development of vaccines to address the “blowback” of the use of biological weapons in war.

I began this research paper in January of this year and, as you’ll see below, the paper has become lengthy and complicated.

I have made the difficult decision of sharing this draft so my readers benefit from the knowledge I’ve compiled thus far as well as my own interpretations of vaccine package insert statements because after reading “The Wuhan Cover Up” I don’t have a timeline for when the final version of the paper below will be complete.

My intention is to complete my review of “The Wuhan Cover Up” and then return to heavy amounts of reading to complete this paper.

Non-Clinical Toxicology sections on vaccine package inserts actualizes latest vaccine discourse with novel implications on the safety of vaccines unknown genotoxic and carcinogenic effects; lack of mutagenic and carcinogenic safety tests for single, multiple, and cumulative doses of vaccines; claims as to vaccines not causing autism or other diseases known to man, the impact on informed consent, lack of justification for not conducting vaccinated versus unvaccinated studies, and other extensions to present-day medicine with absent Non-Clinical Toxicology safety tests [1, 2].

Logical Fallacy of using a Risk-Benefit Ratio Analysis in the Context of Non-Clinical Toxicology Mutagenic/Carcinogenic Safety Tests for any pharmaceutical, such as vaccines: if a person claims the benefit of being vaccinated against a disease outweighs the risk of genetic/carcinogenic effects, there are various assumptions to address: 1. the assumption that the mortality rate of the disease being vaccinated against is higher than other diseases with their own mortality rates where genetic susceptibility to those diseases may be increased via vaccination, 2. the assumption that the cost of treating a disease resulting from genetic damage is less than the cost of treating the disease the person is being vaccinated against, 3. the assumption that potential genetic mutations arising from vaccines are not passed onto the vaccinated person’s offspring via germline mutations (egg/sperm), subsequently impacting numbers 1 and 2 for the offspring prior to considering offspring exposure to additional vaccines, 4. the assumption that “vaccine-induced herd immunity” against one disease outweighs the collective effects of 1 through 3 for all known diseases; 5. the assumption of zero vaccine-derived cases for live-vaccines creating a secondary line of effects for numbers 1 through 4 due to the genotoxicity of an infection itself. There is no ratio of Risk-Benefit in the context of mutagenic/carcinogenic safety tests: it’s zero, there can be zero genotoxic/carcinogenic effects.

The USA-HHS and WHO’s Lacking Empirical Evidence for Not Conducting Mutagenic/Carcinogenic Safety Tests

Since 1996 USA’s HHS/FDA has provided industry guidance on genotoxicity safety tests for biological products, even discussing potential germ cell mutations (i.e., sperm and egg cells). In 1997, HHS recommended the standard 3-test battery for genotoxicity for biological products, and for germ cell mutations states “Nevertheless, because germ line mutations are clearly associated with human disease, the suspicion that a compound may induce heritable effects is considered to be just as serious as the suspicion that a compound may induce cancer. In addition, the outcome of such tests may be valuable for the interpretation of carcinogenicity studies.” The 2010 document states, “Results of comparative studies have shown that, in a qualitative sense, most germ cell mutagens are likely to be detected as genotoxic in somatic cell tests so that negative results of in vivo somatic cell genotoxicity tests generally indicate the absence of germ cell effects.”

However, in 2006 HHS backtracked and stated “Genetic toxicology studies are not needed for biologic or drug/biologic combinations.” Oddly, there are no citations in the 2006 document to reference regarding the genetic safety of biological products to support conclusions that such studies are not needed, and pharmaceutical developers are told to defer to other data via the statement, “…not necessary, provided that adequate studies of the individual drug substances have been conducted.” Which “adequate studies” and are they equivalent to genotoxicity/carcinogenicity safety tests for single, multiple, and cumulative doses of vaccines?

The HHS 2010 industry guidance document states that for vaccine adjuvants “particular studies can be abbreviated, deferred, omitted, or added.” The HHS 2012 industry guidance document states, “The focus of this guidance is testing of new small molecule drug substances, and the guidance does not apply to biologics.” The most recent 2023 industry guidance document states “Assessment of the mutagenic potential of impurities as described in this guidance is not intended for the following types of drug substances and drug products: biological/biotechnological, peptide, oligonucleotide, radiopharmaceutical, fermentation products, herbal products, and crude products of animal or plant origin.”

What changed in the decade from 1996 to 2006? Did such safety tests secretly occur after 1996 but due to negative outcomes reported to the HHS-FDA was the recommendation withdrawn?

World Health Organization (WHO) documents actually paint a similar picture, however the FDA’s industry guidance 1996/1997 documents predate the earliest WHO documents regarding genotoxicity tests, where in 2005 the WHO was already stating genotoxicity studies are not needed for whole-vaccines.

The WHO has been previously criticized in this library for poor autism literature reviews, analysis of ‘autism prevalence’ in age groups without factoring ‘age at diagnosis,’ not providing a global updated strategy for autism spectrum disorders since 2014, warning countries against pregnancy Valproate product use since 2015 due to developmental outcomes without specifying the autism-valproate connection as indicated on FDA inserts since 2011, providing the South-East Asia region a regional strategy for addressing autism rates based upon a cited study that indicated South-East Asia autism rates of less than 1 in 100 among 5-14 year olds in 2010 when in the USA 2010 autism rates were 1 in 68, five Autism Developmental Disabilities Monitoring Network (ADDM) publications that found slightly higher case counts for autism that found higher incidence rates using previous criteria for autism, as well as other criticisms, such as contradictions in statements regarding individuals with developmental disabilities both living longer yet also subject to increased mortality [19].

Okumoto et al. (2023) conducted a review summarizing previous European Medicines Agency (EMA) and World Health Organization (WHO) recommendations regarding Non-Clinical safety tests for vaccines [17]. This review is based upon the country of Japan’s own initiative to revise their guidelines on Non-Clinical safety tests for vaccines by establishing standards based upon available literature. Notable is that the review cites an old 2004 EMA guideline and WHO guidelines published in 2005 and 2014.

Why has the WHO not published new Non-Clinical safety test guidelines for vaccines for over a decade after the exponential increase in adverse event reports after the introduction of Covid-vaccines?

On their site, EMA states that they will not be updating their 2004 non-clinical guidelines for vaccine adjuvants because they’ve been superceded by the WHO 2014 guidelines.

The WHO’s page on Non-Clinical evaluation of vaccines references researchers to the same 2005 and 2014 guidelines discussed by Okumoto et al. (2023), although I happened upon another WHO publication of 2007.

In regards to genotoxicity safety tests, the WHO 2014 guidelines reference their own 2005 guidelines when stating that such studies are not needed for vaccines, a departure from 1997 HHS guidelines that indicated genotoxicity tests for biological products.

However, the 2005 WHO guidelines provides no citation-based scientific support for the identical statement that genotoxicity studies are not needed for vaccines.

Only for the testing of new adjuvants and additives does the WHO 2005 guideline recommend in vitro tests and a full battery of tests for genotoxicity, referencing researchers to a 1997 EMA publication guidelines that mirror the 1997 USA-HHS genotoxicity guidelines. These do not provide guidelines for genotoxicity safety tests for vaccines, but for general genotoxicity safety tests. This explains why one organization’s FOIA requests to the NIH and CDC resulted in neither agency providing safety studies for the injection of aluminum adjuvants in use since the 1930s as indicated by a 2019 NIH response and a same-year CDC response prior to the USA’s withdrawal from the WHO in 2025.

How can government health agency representatives make the statement “vaccines are safe” without knowing if biological products are ‘genetically safe’?

The WHO recommendation to only test new adjuvants and additives after 2005 seemingly discourages genotoxicity/carinogenicity tests of the vaccine-additive thimerosal which has been used in vaccines since the 1930s but has been removed from most childhood vaccines in the USA since 2001 -with certain flu vaccines still containing thimerosal to this day and thimerosal vaccines being sent to low and middle income countries instead, although there is USA funding-pressure for this practice to be phased out from other countries under the current USA administration. The association between thimerosal and autism continues to be part of vaccine-discourse but is not the focus of this review, as Non-Clinical Toxicology safety tests for whole-vaccines is a slightly different discussion regarding genotoxicity/carcinogenicity tests for single-adjuvants (e.g., aluminum salts) or single-additives (e.g., thimerosal) alone. While some studies do find an association between thimerosal and autism while others don’t and the matter is controversial, a yet more conservative approach is to evaluate the whole-vaccine for mutagenic/carcinogenic potential as any associative effect found via alternative studies may be magnified or validated by the whole-vaccine undergoing such evaluative safety tests that directly establish causality (e.g., since a vaccine does not solely contain thimerosal, whole-vaccine mutagenic/carcinogenic safety studies provide a bigger picture). This does not invalidate current findings regarding thimerosal and an association with autism, but rather may validate them through studying potential genotoxic/carcinogenic effects of the whole vaccine via the logic of “well, if the entire thing is found to be genotoxic/carcinogenic, then none of the ingredients are good and why are we using any of them. Let’s start over.” As it stands, because of pressure regarding thimerosal and the longstanding Simpsonwood scandal (the Verstraeten et al. 2000 matter) brought to greater public awareness by the current secretary of HHS, it was removed from most vaccines in the USA in the early 2000s. But is removing and changing vaccine excipients over and over due to findings regarding specific ingredients creating an unethical cycle of medical trial-and-error? Isn’t it more scientifically ethical to evaluate the whole-vaccine to ascertain vaccine-entirety genotoxicity/carcinogenicity rather than reducing arguments to individual components of vaccines?

How does the USA’s withdrawal from the WHO impact internal USA health agencies decisions to conduct such tests or fund the research for such tests in order to assure the public that vaccines are “safe” as per marketing of a vaccine-entirety as “safe”?

Unfortunately, neither do the 2007 WHO guidelines provide citations to scientifically support the statement that genotoxicity/carcinogenicity studies are not needed for DNA vaccines.

In regards to carcinogenic safety tests, the 2014 WHO guidelines state “carcinogenicity studies are generally not needed for adjuvants or adjuvanted vaccines,” also without referencing studies and simply stating it is “based on previous experience.” As previously mentioned, the 2007 WHO guidelines states carcinogenicity studies are not applicable to DNA vaccines, doing so without without citation, and the 2005 publication echoes previous statements that such studies are only needed for new adjuvants or additives.

Based upon this, it can be concluded that the foundations for not conducting Non-Clinical genotoxic and carcinogenic safety tests for vaccines is lacking empirical evidence and scientific basis. While USA health agencies may have been following WHO guidelines regarding not conducting genotoxicity/carcinogenicity safety tests for the entire vaccine and it could explain the HHS’s 2006 backtrack to no longer recommend such safety tests for biological products, there is no scientific basis to support the statement that “biological products (i.e., vaccines) are genetically safe.”

Those who claim that vaccines or biological products are “safe? or “genetically safe” can be requested to provide that research to support the claim.

Previously addressed was lack of external validity should Non-Clinical Toxicology mutagenic/carcinogenic tests be designed to conduct vaccine-to-vaccine comparisons [1], or single-vaccine designs with no external validity to clinic scenarios of multiple doses of vaccines in a single doctor’s visit or cumulative exposure to vaccines across a life span -as in the case of the childhood immunization “schedule” or extensions thereof (e.g., employer requests, “emergency” mandates, international travel requirements, etc.) [2].

Okumoto et al. (2023) comes to various conclusions regarding the design of non-clinical safety tests. However, it is worth noting they do not specifically discuss genotoxicity/carcinogenicity tests for adjuvants/additives or the whole-vaccine.

Do vaccine researchers consider genotoxicity and carcinogenicity safety tests at all?

Some do…as Merck researchers in 2012 published “Strategies for the Nonclinical Safety Assessment of Vaccines” and recommended genotoxicity studies for new adjuvants via citing the 1997 EMA guidelines for such safety tests -the same guidelines the 2005 WHO paper referenced. No recommendations for genotoxicity and carcinogenicity studies for whole-vaccines were recommended in their paper, however [18].

Research question: How much external validity do adjuvant/additive-alone studies carry to whole-vaccine genotoxicity/carcinogenicity studies? Similarly, as previously questioned, how much, if any, external validity do single-whole-vaccine genotoxicity/carcinogenicity studies carry to multiple-whole-vaccine-doses in a single administration and cumulative-whole-vaccine-lifespan-doses?

Some states in the USA are independently re-entering the WHO; albeit, perhaps without awareness of Non-Clinical Toxicology sections of vaccine package inserts regarding genotoxicity/carcinogenicity. The current HHS administration is being sued for attempting to change the vaccine schedule in spite of the American Academy of Pediatrics (AAP) inability to defend claims that vaccines do not mutate genes or increase the risk of cancers. If the AAP believes vaccines do not mutate genes or increase the risk of cancers, they should be asked to provide those whole-vaccine genotoxicity/carcinogenicity safety studies on single, multiple, and cumulative-lifespan (i.e., childhood schedule and extensions) doses to support those claims.

Vaccine-Derived Cases and “Outbreaks”

The CDC defines an live attenuated vaccine (LAV) as, “A vaccine in which a live virus is weakened (attenuated) through chemical or physical processes in order to produce an immune response without the severe effects of the disease. Attenuated vaccines currently licensed in the United States include measles, mumps, rubella, varicella (chickenpox), rotavirus, yellow fever, smallpox, and some formulations of influenza and typhoid vaccines.”

“LAVs act by causing self-limited infections with weakly virulent vaccine pathogens, thereby establishing a long-term immunological memory against specific antigens common to the more virulent parental pathogen. However, LAV infections are not self-limited in all individuals. In rare cases LAVs can cause life-threatening infections that are fatal or could be fatal without modern medical intervention.” [3]

Let us for a moment consider the weight of this publication that explicitly declares a live-attenuated vaccine may cause a life-threatening infection that could be fatal; for the public unaware of the realities of vaccine injuries, or unwilling to address them, this is a matter of scientific inquiry published in the literature.

The National Childhood Vaccine Injury Act (NCVIA) of 1986 explicitly states ‘injury or death‘ may be consequences of various vaccines.

Additionally, the CDC publicly states, “…there is a very remote chance of a vaccine causing a severe allergic reaction, other serious injury, or death.” This statement is found for 26 vaccines on a public CDC page titled ‘Possible Side Effects from Vaccines‘ [20].

Thus, can be laid to rest arguments regarding deaths arising out of vaccines being “anti-vax rhetoric,” “conspiracy theory,” or other scientifically undermining labels. If the CDC page states ‘death’ may be a consequence of 26 different vaccines, then it is a matter of scientific inquiry. If a person “dies suddenly,” then it is a matter of scientific inquiry to examine post-vaccination adverse events and other relevant data to ascertain a potential causal link to vaccines to maintain scientific integrity. If there is a case of Sudden Infant Death Syndrome, then it is a matter of scientific inquiry to examine post-vaccination adverse events and other relevant data to ascertain a potential causal link to vaccines to maintain scientific integrity.

Through the course of writing this paper, I hypothesized the existence of a Linguistic Fallacy of Mutual Inclusivity, where Event = Event-Probability are treated as mutually inclusive (aka, equal to each other) when they are in fact mutually exclusive (Event ≠ Event-Probability) [22-25].

If the CDC website states there is a “remote chance” of “serious injury or death” for those 26 vaccines, then for each of those vaccines:

Hypothesized Equation…
Serious Injury/Death (SID) = Event
Not-SID = Not-Event
Remote Chance = Probability
Probability of SID ≠ Zero Probability
Safe = Zero Probability
Safe ≠ Remote Chance (Probability) of SID
Zero Probability ≠ Remote Chance, because Remote Chance = Probability
SID ≠ Injury/Death-Probability
SID = SID Events / SID Events + SID Not-Events
Therefore, SID events establish the probability of SID events and are mutually exclusive from each other.

What are the ‘informed consent’ implications for these 26 vaccines given these statements on the CDC website?

What are the implications for these 26 vaccines concerning vaccine hesitancy research? If the NCVIA states vaccines may result in injury or death and is the basis for providing vaccine manufacturers liability immunity from injury or death arising from vaccines subsequently approved, and the CDC website states those 26 vaccines may result in ‘injury or death,’ how can a person not be “vaccine hesitant” against a product that the CDC and NCVIA state may result in ‘injury or death’? How can such “vaccine hesitancy” research be conducted in this context? The field of Psychology and its branches will need to address this matter seriously as the statements ‘injury or death’ by the CDC and NCVIA contradict claims regarding vaccine-safety and thereby undermine statements against the hesitation to take a product that may result in ‘injury or death.’ Additionally, the very act of calling it “vaccine hesitancy” may already bias the researchers conducting those studies.

If a government health representative claims “vaccines do not result in death,” then they can be asked why the CDC website makes that statement for 26 vaccines if the CDC website is supposed to be an amalgamation of the vaccine literature in order to market vaccines as ‘safe.’

Non-Clinical Toxicology sections of vaccine package inserts provide new context: government health agencies, and actually no one else for the matter, can defend the claim that vaccines -whether single, multiple, or cumulative doses- do not result in ‘genetic-injury.’

Back to Vaccine-Derived “Outbreaks”: The Logical Fallacy of Touching A Transmittable Virus

Vaccine-derived polio is a matter that has gained warranted attention from both the WHO and the CDC.

In this case of vaccine-derived polio in Rockland County, New York of 2022, the CDC makes statements on vaccine-derived poliovirus.

Research questions based upon these CDC statements regarding vaccine-derived poliovirus:

• What are the contact transmission rates from and to people with immunodeficiency disorders shedding live virus/bacteria due to either vaccination with a live vaccine or contact with another person vaccinated with a live vaccine -for all live virus/bacteria vaccines?
• What are the parameters to classify an immunodeficiency disorder within the context of virus replication, virus shedding, and contact transmission?
• What are the lowest parameters of ‘immunodeficiency’ that extend beyond formal diagnosis but that impact virus shedding and contact transmission due to live-virus/bacteria vaccination?
• How do environmental toxins (e.g., air pollution, pesticides, etc.), nutrition (e.g., malnutrition, organic-nonGMO nutrition, etc.), or drug interactions (e.g., pharmaceuticals that impact the immune system) impact virus replication, virus shedding, and contact transmission due to live-vaccine vaccination among people with or without immunodeficiency (formal diagnosis or lowest parameters extending beyond formal diagnosis that may impact virus replication and virus shedding)?

Above, the WHO states the case of vaccine-derived polio in Rockland County New York was a circulating vaccine-derived polio virus type 2 that resulted in paralysis. The WHO states “the case had no recent history of international travel” and that it the virus was genetically linked to sewage samples in the United Kingdom and in Israel.

How did the individual in Rockland Country contract cVDPV2? Did someone from outside of the USA have contact with a vaccinated individual traveling back into the USA that resulted in contact-transmission?

The matter of vaccine-derived polio outbreaks is not without its controversy. “Thus, VDPV has replaced the wild-type virus as a major threat to global heath.” [3]. “Vaccine safety should also be re-defined to include any serious disease (such as polio), disability (such as incurable paralysis of polio), or death (considering that polio has a case-fatality rate of 10%) among bystanders caused by the spread of the vaccine virus to them, as illustrated by cVDPV-caused outbreaks.” [5]

Even World Health Organization data support these concerns. The most recent WHO polio committee of March 2026 reported only 40 cases of wild polio virus type 1 in 2025 and 99 cases in 2024 (a total of 139 wild polio type 1 cases in 2024 and 2025), in comparison to 202 vaccine-derived polio virus cases in 2025 and 463 in 2024 (a total of 665 VDPV cases across those same two years, of which 640 are cVDPV2 according to WHO data) [20]. Wild type polioviruses 2 and 3 are believed by the WHO to have been entirely eradicated, as they have not detected type 2 since 1999 or type 3 since 2000.

Have vaccine-derived polio outbreaks indeed replaced wild-type as the major polio threat in light of the WHO March 2026 report for endemic wild polio only occurring in 3 countries (Afghanistan, Pakistan, and Germany) in comparison to the 26 countries for vaccine-derived polio type 2, five countries for vaccine-derived polio type 1, and three countries for vaccine derived polio type 3?

Why are most of the cases of vaccine-derived polio type-2?

In the 2022 WHO Position Paper on polio noted above, the WHO admits that when there was a global switch from the trivalent polio vaccine (tOPV) which contains all 3 types of polio viruses to the bivalent live-polio vaccine (bOPV) containing only types 1 and 3, cases of circulating vaccine-derived polio type 2 (cVDPV2) increased in number instead of decreasing.

However, in 2016 a CDC publication on vaccine-derived polio viruses made the statement that “…the global cessation of tOPV use is essential for eliminating cVDPV2s…” The CDC also stated in that 2026 publication, “Any tOPV found in a vaccine storage refrigerator or freezer in the future should be destroyed…”

The CDC was undoubtedly following the 2016 WHO recommendation to cease use of the tOPV vaccine and to destroy tOPV vials, as well as the destruction of monovalent mOPV2 vials after vaccination in an effort to prevent cVDPV2s. The 2016 WHO paper also recommends destruction of type 2 poliovirus strains held at research and manufacturing facilities used in creating the tOPV and mOPV2 vaccines, this recommendation made in order to prevent polio outbreaks.

However, in the same 2016 document, the WHO also states that if an outbreak of type 2 poliovirus occurs, without specifying whether it is vaccine-derived or wild type outbreak, there is a global stockpile of 50 million mOPV2 doses assembled in preparation. [29]

The mOVP2 is also a live-vaccine containing only type 2 vaccine-derived poliovirus.

The WHO 2022 polio paper provides the statistic of 1,804 paralytic cases due to circulating vaccine-derived poliovirus. This is stark contrast compared to only 146 wild-poliovirus cases for the years 2020-2021.

How could the CDC and the WHO have been wrong that global cessation of tOPV use was essential for eliminating cVDPV2s? A 2024 publication by the CDC, pictured previously, indicates that large cVDPV2 outbreaks were occurring in Africa as early as 2017, merely a year after the recommendation to cease tOPV.

The 2025 publication by the CDC discussing the detection of vaccine-strain poliovirus type 2 in wastewater of 5 countries in Europe states “Because most polio infections are asymptomatic and polioviruses are shed in stool, many countries in Europe supplement syndromic AFP and enterovirus surveillance by conducting environmental surveillance (ES) for polioviruses through the systematic sampling of wastewater.” While the 2025 CDC publication indicates no human polio cases were reported in association with those wastewater detections, this does not mean asymptomatic infections did not occur that resulted in the shedding of VDPV2 in the stool. Is not polio virus infection (either wild or vaccine-strain), whether symptomatic or asymptomatic, the very requirement for polio virus stool shedding? In the case of vaccine-derived polio virus detection in the wastewater of five European countries as noted in that CDC publication, that wastewater detection is traced back to live-vaccine vaccination that resulted in the transmission of a vaccine-strain to individuals in Europe that later shed the virus in their stool but most likely were asymptomatic as evidenced by there not being formal human polio cases or poliovirus infections associated with that wastewater VDPV2 detection.

After CDC and WHO recommendations to destroy tOPV vials, why does the WHO in 2022 state that the tOPV can be used in an outbreak response when the CDC and the WHO in 2016 both said tOPV found in vaccine storage should be destroyed? The WHO even provides countries an application for tOPV, and in the 2022 paper states, “Any type 2-containing OPVs (tOPV or mOPV2) are used exclusively in outbreak response to type 2 poliovirus.”

The CDC and WHO blame lack of vaccination for the increase in vaccine-derived outbreaks and this was echoed in the 2016 CDC’s paper that indicated “cessation of tOPV use carries some risks for facilitating the spread of undetected or newly emergent cVDPV2s among persons without immunity to type 2 poliovirus infections after the switch to bOPV.”

The 2016 WHO paper made a nearly identical statement: “Although the global cessation of tOPV use is essential for eliminating cVDPV2s, it carries some risks in facilitating the spread of undetected or newly emergent cVDPV2s among persons without immunity to type 2 poliovirus infections after the switch.”

So, both the WHO and CDC knew cessation of tOPV could result in new cVDPV2s and the latest polio committee of March 2026 indicates that in the years of 2024 and 2025 there was more than 4 times more circulating vaccine-derived polio type 2 than there was wild type polio 1, the CDC in 2024 reported that vaccine-derived polio outbreaks for type 2 happened as early as 2017 merely a year or less than the worldwide recommendation to cease tOPV, and now the WHO is recommending tOPV for an outbreak response to vaccine-derived polio type 2…?

What is the logical basis for the 2022 WHO position paper saying lack of vaccination for type 2 vaccine-derived polio is the culprit behind increasing vaccine-derived cases for type 2 when the CDC and the WHO recommended worldwide cessation of tOVP containing type 2?

In other words, if the CDC-WHO recommended cessation of tOVP which contains 3 strains of polio viruses in favor of the bOPV which only contains types 1 and 3, what is the logical basis for the 2022 WHO paper saying lack of vaccination using the monovalent type 2 polio vaccine (bOPV) is the culprit AND when the bOPV vaccine can also result in type-2 vaccine-derived cases as indicated by transmission statements on the bOPV vaccine package insert? The same is true for the nOPV insert regarding possible transmission resulting in vaccine-derived type 2 polio cases, where the WHO 2022 polio paper recommends nOPV to respond to type 2 cases: “In November 2020, type 2 nOPV (nOPV2) was recommended under WHO Emergency Use Listing (EUL) for outbreak response to cVDPV2s.”

This is a logical fallacy where vaccinating results in vaccine-derived cases yet simultaneously NOT vaccinating is blamed for vaccine-derived cases. How can lack of vaccination be the culprit for polio outbreaks and vaccination result in polio outbreaks?

“Hypothesis: Not-Vaccine Disease Never Equals Vaccine-Disease Probability
If Vaccine then Disease,
then Disease-Probability from Vaccine,
because Disease-Probability = Disease / Disease + Not-Disease and because Not-Disease ≠ Disease.

If Vaccine then Vaccine-Disease (aka Vaccine-Strain Case),
then Vaccine-Strain Case Probability from Vaccine,
because Vaccine-Disease Probability = Vaccine-Disease / Vaccine-Disease + Not-Vaccine Disease and because Not-Disease ≠ Disease.” [24]

Let’s apply this to vaccine-derived polio:
Vaccine-Derived Polio-Virus (VDPV) ≠ No VDPV
VDPV ≠ VDPV-Probability
VDPV-Probability = VDPV / VDPV + No-VDPV
Thus, VDPV is mutually exclusive from VDPV-Probability because there is no probability of VDPV without VDPV events, and VDPV events by definition are vaccine-derived due to vaccine-strain viruses.

Rewritten: How can lack of vaccination be the culprit for [wild] polio outbreaks and vaccination result in [vaccine-derived] polio outbreaks?

Rewritten 2: How can lack of vaccination be the culprit for [vaccine-derived] polio outbreaks and vaccination result in [vaccine-derived] polio outbreaks?

The WHO reports in March 2026, “Since its introduction in 2021, more than 2 billion doses of nOPV2 have been administered and a total of 42 cVDPV2 emergences have been associated with it. The Committee noted that nOPV2 continues to demonstrate significantly greater genetic stability and a substantially lower risk of reversion to neurovirulence compared to Sabin OPV2. More than 80% of cVDPV2-affected countries have interrupted outbreaks with three or fewer SIAs using nOPV2.”

If one goal of live-vaccine research is to genetically stabilize viruses used in vaccines to lower the risk of reversion to neurovirulence in order to decrease vaccine-derived cases, does this not in itself implicate decades of live-vaccine usage as experimentation at the cost of vaccine-derived cases and at the cost of viruses regaining neurovirulence in a host and in a population due to contact transmission (either the vaccinated host or the person that came into contact with the host)? [Logical fallacy arguably being the contention that the immune system of the person isn’t supposed to permit a virus regaining virulence because their immune system is supposed to fight it off; places logical burden upon the immune system and blame for vaccine-derived cases onto the populace/person, moving scientific responsibility from the vaccine-maker to the person, a layer 2 issue because the layer 1 presumption was in the use of a virus to begin with which could result in transmission.]

Do we really understand “flu seasons” in the context of live-virus flu vaccines which first became in use in the 1930s? [21] How much have flu vaccine-strains mutated since then and how are flu viruses sequenced each year to create new flu vaccines, as per CDC statements regarding flu genome sequencing? Are flu vaccines created based upon mutated vaccine-derived cases? Are we in a cycle of undisclosed vaccine-derived flu outbreaks?

CDC documents obtained via FOIA request revealing the CDC’s genotyping of a measles strain to determine a vaccine-derived case [4], as well as the CDC’s project of genome sequencing of flu viruses since the 1980s with a 2024 page by the CDC noted above indicating that in 2017-2018 more than 1 million flu virus specimens obtained from patients underwent testing as well as the statement that in a typical year the CDC analyzes about 7,000 flu viruses, indicate that the CDC is perfectly capable of detecting vaccine-strain viruses/bacteria for all live vaccines.

Genetic sequencing is how the WHO detects vaccine-derived strains of polio, and they published in 2022 strategies on global genomic sequencing “for pathogens with pandemic and epidemic potential,” a moot document in light of any virological research, especially gain-of-function research, involving the containment of viruses in laboratories, for how can countries and their scientists/researchers be requested to prepare for pandemics/epidemics while virus research is conducted that may result in virus pandemics to begin with? The matter brings us back to the WHO and CDC’s request for the destruction of tOPV vials containing live viruses for polio types 1, 2, and 3, as well as the recommendation to and destroy mOPV vials to reduce outbreaks after vaccinating an individual.

Government institutions may laud themselves for their efforts in “preparing” the public for pandemics/epidemics, but as long as the study of viruses continues where viruses themselves are contained in laboratories and there is a risk, however small, of transmission and epidemics traced back to laboratories, how can any institution provide such guidelines? If a government permits the studying of viruses within its borders (or funds such research outside its borders), and in some cases permits gain-of-function research that involves increasing virulence, transmissibility, and host-range, how can the same government provide guidelines for preparing for pandemics/epidemics when they themselves are permitting such research thereby risking pandemics/epidemics?

In the context of vaccines, would government health agencies hide vaccine-derived cases that might be infectious and result in transmission to others, subsequently resulting in an “outbreak”?

Vaccine-Derived Cover Ups and Implications

The CDC does publicly acknowledge vaccine-derived cases of yellow fever, as in the case of seven cases of yellow fever vaccine–associated viscerotropic disease (YEL-AVD) in 2001, and the WHO in 2008 also made a statement regarding YEL-AVD, collectively acknowledging such vaccine-derived cases.

However, it appears the public is not always at the receiving end of CDC transparency regarding vaccine-derived cases.

For example, government health agencies did not declare to the public that a measles case in Maine of 2022 was vaccine-derived. However, internal CDC documents obtained through Freedom of Information Act by an organization explicitly confirm the measles case was ‘consistent with vaccine strain’ [4].

The internal CDC document contradicts Maine of CDC statements in May of 2023 that, “The child received a dose of measles vaccine. It is not possible to contract measles from the vaccine. Maine CDC is considering the child to be infectious out of an abundance of caution.”

Collectively, the initial statements by the CDC of Maine and internal CDC documents obtained through FOIA elucidate that a vaccinated child was infectious for a disease they were vaccinated against/for.

A few weeks later, the Maine of CDC backtracked and stated the child was not infectious. However, there is a newfound query: what is the scientific foundation for stating someone receiving a live-virus vaccine containing a replicating virus may not be or become infectious?

Failure to disclose a vaccine-derived cases carries other implications: how many vaccine-derived “cases/outbreaks” have not been previously disclosed to the public and what is the ethics foundation that is the basis for not disclosing these cases? If the CDC internally opted for not disclosing a vaccine-derived measles case, researchers should presume there is a published scientific literature on the ethics for not disclosing vaccine-derived outbreaks. However, the internal CDC document states, “Disclaimer. These results are intended for public health purposes only and must NOT be communicated to the patient, their care provider, or placed in the patient’s medical records. These results should NOT be used for diagnosis, treatment, or assessment of patient health or management.” [4]

To my knowledge, there isn’t a published literature on the ethics of disclosing or not disclosing vaccine-derived outbreaks to the public, and surely a FOIA request requesting published studies that could be the basis for such internal CDC decisions would yield no results. Perhaps this is because open discourse on vaccine-derived cases for illnesses is expected to impact vaccine hesitancy, moot contentions under the context of lacking genotoxicity/carcinogenicity safety tests.

From this CDC internal document are new research questions:

• Do patients have a right to know that their diagnosis of a disease case was vaccine-derived?
• Should vaccine-derived cases be placed in a patient’s medical records?
• If there is a case of vaccine-derived disease, are there ethics violations of not disclosing that information to researchers that could result in assumptions that all cases of a disease publicly discussed are wild-type and not vaccine-strain?
• If such information is withheld due to concerns of increased “vaccine hesitancy,” what base does that contention have in the context of absent mutagenic/carcinogenic safety tests for vaccines?
• Why are ‘consistent with vaccine strain’ results not used for diagnosis, treatment, or assessment of the patient’s health or management when it already impacted the patient’s health via diagnosis of their vaccine-derived case? Is this because the pre-determined solution is to advocate for greater vaccination (a hypothesized logical fallacy as it concerns live-vaccines because they can result in vaccine-derived cases)?
• Historically, how many vaccine-derived cases of measles, mumps, rubella, varicella, rotavirus, yellow fever, smallpox, influenza, typhoid, and polio have been identified by government health agencies since these live-vaccines have been in use?

Can there ever be an ethical basis for not disclosing a vaccine-derived case to a public, or even to a patient, that deserves informed consent and government health agency transparency? Does not the patient have a right to know there are vaccine-derived cases, historically, as a part of their informed consent for receiving a vaccine?

There are published case reports regarding vaccine-derived cases, such as a 2022 case report of vaccine-derived rubella in an immune-compromised individual. Was their diagnosis due to the vaccine? Yes, the report states they had received 2 MMR vaccines…when they were an infant. The publication is in regards to a 20 year old diagnosed with vaccine-derived rubella -more than 15 years after vaccination with MMR. “Because the patient had no known recent exposures to persons with suspected or confirmed rubella, there was concern that the RuV had been acquired earlier, potentially through MMR vaccination. The complete genomic sequence of the isolated virus was determined using the Sanger method and designated RVi/Oregon.USA/49.20 (GenBank accession number ON861827). Phylogenetic analysis showed that the isolated virus was vaccine-derived with 97.3% nucleotide identity to the genomic sequence of the RA27/3 strain used in an MMR vaccine. A 36-nucleotide deletion in RVi/Oregon.USA/49.20 resulted in the N-terminal deletion of 12 amino acids of the E2 glycoprotein. Despite this deletion, the virus replicated efficiently in Vero cells, producing titers around 10⁶ focus forming units (ffu) per mL of the culture medium, which is 1–2 logs higher than those produced by other previously described VDRV isolates.” [7]

Researchers stated, “the prevalence, persistence, and transmissibility of vaccine-derived rubella virus (VDRV) infection have yet to be fully elucidated” [7]. In other words, the researchers themselves lacked scientific evidence to make assertions regarding how often vaccine-derived rubella cases are occurring, and they lacked evidence to form a scientific foundation for how vaccine-derived rubella can be transmitted from one individual to another. The authors concluded, “Though the absence of transmission to close, vaccinated contacts in the current setting is reassuring, we cannot rule out the possibility that VDRV might be transmitted from such a patient to unvaccinated pregnant people, their fetuses, and infants 6–12 months of age, after waning of maternally acquired antibody but prior to receipt of MMR, as reported elsewhere.”

The researchers conclusion that lack of vaccination against rubella is protection from vaccine-derived outbreaks is a logical fallacy to begin with. Is the supposed solution against vaccine-derived cases just more vaccination with live-vaccines that can result in vaccine-derived cases?

Hypothesized Logical Fallacies of the Live-Vaccine “Science” Foundations

“The virus in the oral type of the vaccine is also excreted in faeces. Mass campaigns using oral polio vaccine interrupts WPV [Wild Polio Virus] circulation by boosting population immunity so that transmission of poliovirus cannot be sustained. When a child is immunized with Oral Polio Vaccine (OPV), the weakened vaccine-virus replicates in the gut for a limited duration, and as immune system is stimulated, it develops antibodies against the virus. In areas of crowding and inadequate sanitation, this excreted vaccine-virus undergo some replication and can spread in the community, which also protects other children through ‘passive’ immunization. But if a population is significantly under-immunized, the excreted vaccine-virus circulates for a longer period of time (at least 12 months) and it undergoes many genetic changes. Very rarely, the vaccine-virus can genetically change into a form that can cause paralysis similar to the wild poliovirus and is known as a circulating vaccine-derived poliovirus (cVDPV). cVDPVs occur when routine or supplementary immunization activities are poorly conducted, and population has a low vaccination coverage. Contrarily, if a population is fully immunized, it is safe from both vaccine-derived and wild polioviruses.” [9]

The vaccine virus can evolve and reacquire neurovirulence over the course of 12 to 18 months if it is allowed to circulate for an extended period without interruption. Because of insufficient vaccination coverage, cVDPVs can typically recombine with other enteroviruses increasing their neurovirulence and transmissibility. [9]

In rare cases, OPV can cause vaccine-associated paralytic poliomyelitis (VAPP), which is characterized by acute flaccid paralysis and residual paralysis. [10]

Two rare but serious adverse events are associated with OPV: VAPP and VDPVs. VAPP is an adverse event following exposure to OPV. VDPVs, by contrast, are polioviruses that have atypical genetic properties indicative of prolonged replication or circulation. VAPP occurs among OPV recipients and their contacts, and has been recognized since the licensure and widespread use of OPV in the early 1960s. In instances of VAPP, the attenuated Sabin polioviruses in OPV strains replicate in the intestine and revert to neurovirulent variants that enter the central nervous system and cause paralysis that is clinically indistinguishable from poliomyelitis caused by WPV. In countries using OPV, the risk of VAPP is estimated at 3.8 cases per million births (range: 2.9–4.7, estimated from use of tOPV).

VDPVs are classified into 3 categories: i) circulating vaccine-derived polioviruses (cVDPVs), with evidence of community transmission; ii) immunodeficiency-related VDPVs (iVDPVs), when isolated from persons with PIDs [primary immunodeficiency disorders]; and iii) ambiguous VDPVs (aVDPVs), when isolated from persons with no known immunodeficiency and no evidence of community transmission, or when isolates from sewage are not genetically linked to other known VDPVs and whose source is unknown. Most cVDPVs are recombinants with other enteroviruses and evolve towards a non-temperature sensitive phenotype for growth at 39.5°C. Loss of attenuating mutations allows cVDPVs to regain the neurovirulence and transmissibility of WPV; thus, clinical presentation and epidemiology of paralytic cases is similar for cVDPV and WPV of the same serotype.

Polio vaccines: WHO position paper –JUNE 2022

Returning to the case of vaccine-derived polio detected in Rockland County New York in 2022, the CDC stated that vaccine-derived polio was detected in an unvaccinated individual. The CDC page also states that vaccination against polio protects against natural polio and vaccine-derived polio viruses. However, this carries a logical fallacy: would the polio-unvaccinated individual been at risk of contracting polio to begin with were it not for virus shedding from the recipient of a live virus polio vaccine?

Hypothesized sequence:

1. There are zero vaccine-derived cases of polio in New York.
2. An unvaccinated individual comes into contact with a person who was shedding the virus from the live virus polio vaccine.
3. Due to virus shedding, now there’s a case of vaccine-derived case of polio.
4. Lack of vaccination against polio is blamed for contracting vaccine-derived polio due to someone else’s virus shedding -a False Cause Fallacy.
5. The pre-determined solution is to recommend more vaccination against polio, which layers a solution on top of the False Cause Fallacy subsequently forcing individuals to accept the fallacy as being true. [in the USA since 2000 the inactivated polio vaccines which does not contain live-viruses is used, but this is not so in other countries in light of the WHO’s seemingly-ever-changing recommendations to use varieties of live-virus polio vaccines that may result in vaccine-derived cases in the USA]

Logical fallacies: Exposing a population with a weakened live virus of the disease in a vaccine to protect against the disease, and local feces exposure in a population with poor sanitation is called “passive immunization” via virus shedding in the stools of live virus vaccine recipients, but lack of vaccination among the same or a different population is blamed for the same weakened live virus genetically changing/mutating into a form that can cause the same disease it was meant to protect individuals from and/or recombining with other enteroviruses that increases its neurovirulence and transmission and its no longer called “passive immunization” if this happens because “the virus mutated due to lack of vaccination” and therefore it’s the fault of more people not being vaccinated, and further vaccination is needed to stop transmission of vaccine-derived cases due to virus shedding from the live-virus vaccine which in some instances can also cause the disease itself and those vaccine-derived cases can be clinically indistinguishable from a disease-case of the wild-type (e.g., Poliomyelitis can be caused by the polio virus, and the 3 types of wild polio viruses are used to create polio vaccines which contain live viruses, that virus can sometimes be shed in the stool and result in vaccine-derived cases, but the live-virus vaccine itself can sometimes cause vaccine-associated paralytic poliomyelitis, and also the virus in the polio vaccine can mutate and be transmitted to others if they are not vaccinated against polio, but stopping use of a vaccine that contained 3 strains of polio (tOPV) to only 2 strains of polio (bOPV) resulted in an increase of cases for which there wasn’t the third strain in the bOPV, the polio vaccine is indicated on the CDC website to potentially cause ‘injury or death,’ oh and the National Childhood Vaccine Injury Act of 1986 protects vaccine manufacturers from liability for ‘injury or death’ from vaccines).

Thus, the blaming low immunization rates for an “outbreak” or even a single case that was vaccine-derived to begin with is logical fallacy of False Cause.

Blaming immune compromised individuals for shedding and transmitting a virus/bacteria is another logical fallacy in the context of Non-Clinical Toxicology: lack of mutagenic safety tests for vaccines results in the inability of vaccine manufacturers to rule out the possibility that single, multiple, and cumulative doses of vaccines are not mutating genes that result in immune compromising -and the post-marketing sections of many vaccine package inserts specifically possess immune system disorders in their sections. Live-vaccines may be contraindicated for people with immune system disorders; but lack of mutagenic safety tests do not rule out that vaccines may not result in immune system disorders due to genetic mutations.

[MINDMAP]

Transmission: Live-(Virus/Bacteria) Vaccine Package Insert Statements

Let us now review vaccine package insert statements on transmission that directly support the hypothesis that an individual can transmit the disease they are vaccinated against/for (already supported in the polio literature), which supports statements that an individual can contract the disease they are vaccinated against/for (already supported by the CDC’s Pink Book).

The CDC Pink Book states, “To produce an immune response, live, attenuated vaccines must replicate in the vaccinated person. A relatively small dose of administered virus or bacteria replicates in the body and creates enough of the organism to stimulate an immune response. Although live, attenuated vaccines replicate, they usually do not cause disease such as that caused by the wild form of the organism. When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease and is considered an adverse reaction to the vaccine. The immune response to a live, attenuated vaccine is virtually identical to that produced by a natural infection because the immune system does not differentiate between an infection with a weakened vaccine virus and an infection with a wild virus” [28].

Thus, based upon the CDC’s Pink Book:
1. Virus and bacteria must replicate to induce an immune response.
2. Vaccines can/do result in the disease the person is vaccinated against/for.
3. An adverse reaction to the vaccine is equal to a live-vaccine(disease), where the adverse reaction is the disease itself of the virus.
4. Immune response to live-vaccines is identical to wild-type viruses

“A live, attenuated vaccine virus could theoretically revert to its original pathogenic form. This is known to happen only with live (oral) polio vaccine, which is no longer available in the United States” [28]. This CDC’s Pink Book statement is applicable to additional vaccines, where transmission is possible due to reversion to a pathogenic form, where the CDC’s definition of a ‘pathogen’ is an organism that causes disease, as well as consistency with CDC statements that ‘When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease.”

Transmission Statements Logic: If you can transmit the disease you must have the disease due to enough viral replication from the live-vaccine; thus, you cannot transmit an infectious disease you don’t have. If the CDC’s Pink Book says ‘theoretically” a virus from a live-vaccine could revert to a pathogenic form, then transmission statements on live-vaccines support the statement that they can, making it no longer theoretical.

OPV -Oral Polio Vaccine, the World Health Organization has taken this page down and it’s only available via Archive.org

bOPV -Bivalent Oral Polio Vaccine

tOPV -Trivalent Oral Polio Vaccine

No transmission statements can be found on the package insert for tOPV. If the tOPV has 3 live viruses, then it can be deduced transmission statements and VAPPs statements from other polio vaccines containing either one of these viruses should also apply.

mOPV -monovalent oral polio vaccine

The package insert statement for mOPV, while not directly stating live-virus transmission, states a person in close contact with a vaccinated child may be at risk of VAPP. This statement is a transmission statement; and if transmission is possible, the insert should have included statements on live virus transmission and/or shedding since these are prerequisites for a VAPP to occur, but does not; however, they can be deduced from the transmission statement.

mOPV2

As with the mOPV, this MOPV2 states a person in close contact with a vaccinated child may be at risk of VAPP. The same implications for mOPV are applicable to mOPV2; this statement is a transmission statement; and if transmission is possible, the insert should have included statements on live virus transmission and/or shedding since these are prerequisites for a VAPP to occur, but does not; however, they can be deduced from the transmission statement.

nOPV2 -Novel Oral (nOPV) Monovalent type 2

If the insert for nOPV2 indicates the transmission of virus in the nOPV2 vaccine is “no greater and possibly less” than the Sabin-2 virus, what is the logical/scientific justification for recommending nOPV2 after in 2016 the WHO and CDC recommended the withdrawal of the tOPV which contains Sabin-2 and is confirmed by CDC (see image below)? In other words, why was the withdrawl of a vaccine that contained Sabin-2 recommended while simultaneously recommending the use of vaccines that contain a virus with “no greater and possibly less” transmission rates? If the argument is: because Wild Type 1 and 3 are no longer found in nature and only vaccine-derived type 2, what is the logical sequence for recommending a vaccine that can result in vaccine-derived type-2 to prevent vaccine-derived type-2?

MMRV -Proquad (Live-Virus) Measles, Mumps, Rubella, Varicella

The statement on the MMRV insert, “there are no reports of transmission of the more attenuated Enders Edmonston strain of measles virus.”

As discussed previously, the CDC of Maine had originally stated a child was infectious when they had been recently vaccinated with an MMR vaccine, supporting statements that a person can be infectious for a disease they are vaccinated against/for because of the virus in the vaccine (i.e., if disease transmission for an infectious is possible, it should only be possible if you have the disease). Even though the insert for MMR vaccine states “there are no reports of transmission,” this is not to be equated to the statement “transmission is not impossible.” Once again, transmission of an infectious disease should only be possible if a person is a carrier of the disease (virus), and upon vaccination with a live-vaccine, does that not instantly make an individual a carrier of that vaccines virus(s)?

Unlike the JYNNEOS vaccine which uses a non-replicating virus and does not include statements on transmission, the ProQuad vaccine provides specific guidelines for not giving immune globulins or other blood products because they interfere with “vaccine virus replication.”

This is consistent with the previously-discussed CDC Pink Book statement that, “A relatively small dose of administered virus or bacteria replicates in the body and creates enough of the organism to stimulate an immune response. Although live, attenuated vaccines replicate, they usually do not cause disease such as that caused by the wild form of the organism. When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease and is considered an adverse reaction to the vaccine.”

Why did the CDC of Maine claim that the case report of Measles was “not infectious” when the package insert for ProQuad contraindicates blood products that interfere with virus replication?

If the polio literature indicates that virus replication can occur as a consequence of the Oral Polio Vaccine, and virus replication results in fecal shedding consequently resulting in “passive immunization” -a reasonable conclusion since by CDC definitions a virus is an organism that multiples- are implications regarding virus replication and the contraindication for blood products that interfere with virus replication extended to other live-vaccines [9]?

What is the linguistic difference between “passive immunization” and disease-infection? Hypothesized as none; passive immunization seems to be the same as disease infection, where virus transmission is the linguistic common denominator. The polio literature describes “passive immunization” as coming into contact with the virus that is shed from the vaccinated person [9, 26, 27], thus the polio literatures definition of “passive immunization” actually correlates with the CDC’s Pink Book definition of “active immunity” which is acquired through contracting the disease [28].

“In areas of crowding and inadequate sanitation, this excreted vaccine-virus undergo some replication and can spread in the community, which also protects other children through ‘passive’ immunization” [9].

“Viral shedding has secondary benefits of exposing those unreached by vaccination efforts to virus, potentially providing passive immunization. Our results indicating similar levels of viral shedding to mOPV2 soon after vaccination with nOPV2 candidates, but with generally lower viral shedding more distal to vaccination, offer encouraging signs that the vaccines are replicating in sufficient quantity and duration to generate an intestinal immune response, but are not shed in significantly greater quantities than mOPV2″ [26].

“In non-vaccinated populations, excreted vaccine viruses are transmitted within (and to a lesser degree beyond) households, and “passively” immunize persons not directly reached through immunization programmes” [27].

Research question: if the CDC defines ‘active immunity’ as being acquired through contracting the disease yet the polio literature defines ‘passive immunization’ as also being acquired through contracting the disease due to vaccine-virus shedding, is there a Fallacy of Mutual Exclusivity where immunity is acquired through the singular event of virus-contact and the two types of immunity (passive immunization and active immunity) are not actually mutually exclusive? The transmission statements on live-vaccine package inserts support the extension of implications and questions regarding the meaning of “passive” versus “active” immunization, if a person can transmit a disease they were vaccinated against/for.

Research question: if “passive immunization” is defined in the polio literature as coming into contact with the vaccine virus due to shedding, why did the CDC of Maine blame an unvaccinated individual for contracting polio from a person recently vaccinated with a live polio vaccine instead of calling them “passively immunized”?

Research question: if “passive immunization” is defined in the polio literature as coming into contact with the vaccine virus due to shedding, what are the implications for other live-vaccines and so-called “outbreaks” that may really be group-cases of “passive immunization”? Once again, transmission statements on live-vaccine package inserts support the extension of implications.

Is there a linguistic reconciliation between “Active immunity” and “Passive immunity,” “vaccination w/ live-vaccines” and “contracting a disease”? All four seem mutually inclusive at their core, where they should not be treated as mutually exclusive.

The CDC’s Pink Book does state, “The immune response to a live, attenuated vaccine is virtually identical to that produced by a natural infection because the immune system does not differentiate between an infection with a weakened vaccine virus and an infection with a wild virus” [28]. This is logical, as live-vaccines contain live viruses/bacteria; and this appears to negate treating the terms “Active immunity” and “Passive immunity,” “vaccination w/ live-vaccines” and “contracting a disease” as mutually exclusive.

Based on CDC definitions:
Active(Immunity) ≠ Passive(Immunity), leaving…Active ≠ Passive
However, if Active means contracting a disease, and Passive means the passing of antibody protection…yet based upon polio literature it also means coming into contact with disease from vaccine-strain viruses being shed, then this turns into…
Active Immunity via wild-type virus/bacteria (contact with wild disease) = Passive Immunization (contact with disease via shedding) = Active Immunity (contact with live-vaccine disease)

Is ‘Exposure’ to infectious agents such as bacteria and viruses the common denominator for live-vaccines, passive immunization through contact with viruses via vaccine-virus/bacteria shedding, and contact with wild-type viruses?

MMR-II (Live-Virus) -Measles, Mumps, Rubella

The package insert for MMR-II does not mention live virus transmission, but does include a citation regarding transmission of the mumps virus to the placenta while simultaneously contraindicating MMR-II to pregnant woman or those planning on becoming pregnant.

Why does the package insert include a citation for transmission of mumps, but not provide formal transmission warnings regarding transmission of any virus provided it is a live virus vaccine of 3 different viruses as described in the package insert? Logic: if a virus replicates, and replication is needed to stimulate an immune response as per CDC definitions, replication should then by default create a possibility of transmission.

Priorix -measles, mumps, rubella

The statement, “no documented confirmed cases of transmitted rubella vaccine virus” is not to be equated with ‘never happening’ or ‘zero probability,’ especially if cases of rubella are treated as wild-type or left assumed as wild-type if there is no genetic sequencing to trace potential vaccine-strain origin.

BCG (Live-Bacteria) -Bladder Cancer

Vaxchora (Live-Bacteria) -Cholera

RotaTeq (Live-Virus) -Rotavirus

Rotarix (Live-Virus) -Rotavirus

Vaccinia (ACAM2000) (Live-Virus) -Smallpox and Monkeypox

In the case of the Vaccinia (ACAM2000) package insert, contact-transmission is vaccine-derived cases via contact with live-virus vaccinated individuals, hence the package insert recommendation to wash hands thoroughly after administration of the vaccine.

Auto-inoculation statements highlight that administration of the vaccine itself places the administrator at risk of contracting the live virus independent of contact transmission, which carries implications for safe vaccine administration and vaccine derived transmission independent of contact transmission.

Implications to other live-vaccines and research question: How “safe” is administration of a live virus/bacteria vaccine if auto-inoculation can result in an administrator becoming a carrier of a live virus/bacteria, and can auto-inoculation result in contact transmission from the administrator to other individuals resulting in vaccine-derived cases (e.g, vaccine-derived cases via contact transmission due to unintended auto-inoculation)?

Research question: if live virus vaccine administrators are constantly at risk of contact transmission or auto-inoculation, what are the long-term health effects for administrators of live-vaccines whose immune systems may be required to defend themselves due to repeated exposures that may or may not result in formal diagnosis or symptoms? The package insert states serious complications may follow either “primary or revaccination,” thus, what are the health consequences for vaccine administrators subject to contact transmission or auto-inoculation? These questions can similarly be posed regarding the safety of all live-virus vaccine administrators/administration.

ACAM2000 insert provides the most data on contact transmission in comparison to all other package inserts. Why don’t other package inserts for live vaccines provide similar data on contact transmission or auto-inoculation?

Contact transmission: If the Department of Defense program had 71% primary vaccination in their sample of 730,580, and yet per the data in the table there were 52 contact transmission cases with an incidence rate of 71.18 per million, while the Department of Health and Human Services Program had a 36% primary vaccination percentage in their sample of 40,422 with zero cases of contact transmission, this means the group with higher primary vaccination percentage also had higher contact transmission. This has implications for vaccine-derived “outbreaks” due to contact transmission among high vaccination percentage groups.

Research question: are there higher rates of contact transmission among highly vaccinated groups for live-virus/bacteria vaccines, and how does this change our understanding of vaccine-derived cases or disease “outbreaks”?

Secondary transmission is noted in the Post-Marketing data of the ACAM2000 vaccine.

Above is a ‘Medication Guide’ for ACAM2000 found on the FDA website that further elucidates transmission of vaccine virus, specifically stating hands, bandages, clothes, towels, or sheets in contact with the vaccination sight may be contaminated with the vaccine virus. Noted is the recommendation to throw away gloves, gauze, semipermeable dressing, and bandages in sealed plastic bags and to use bleach to kill the virus. Noted is the recommendation to wash clothes, towels, bedding, and other items that may have come into contact with the vaccination site separately.

JYNNEOS (Live-Virus)- Smallpox and Monkeypox

The package insert for JYNNEOS states it “is a live vaccine produced from the strain Modified Vaccinia Ankara-Bavarian Nordic (MVA-BN), an attenuated, non-replicating orthopoxvirus.” Because the virus is non-replicating, there is no mention of transmission on this package insert.

Vivotif (Live-Virus)- Typhoid

Lack of documentation is not to be equated with ‘zero probability’ or ‘never probable’ without genetic sequencing of virus strains to trace origins to vaccine strain and rule out wild-type strain, or vice versa.

Varivax (Live-Virus)- Varicella (Chickenpox)

Although this insert states some cases may represent wild-type varicella from community contacts or low incidence of transmission of vaccine virus from vaccinated contacts, how are researchers to know this unless each case has genotype sequencing of the virus to ascertain the number of cases for each?

YF-Vax (Live-Virus)

Research question: considering YF-Vax is a live-virus vaccine, why does the insert not include additional transmission warnings and limits the discussion to only contraindication to lactating women?

Do the implications regarding the transmission of vaccine-viruses in breastmilk extend to other live-vaccines?

Adenovirus (Live-Virus)

Research question: can fecal shedding during delivery result in vaccine-virus transmission to hospital staff involved in the delivery or cleaning/disposal of feces?

Research question: is such fecal shedding during delivery resulting in vaccine virus transmission equal to “passive immunization” as per polio literature definitions?

FluMist

Zostavax -Herpes Zoster (shingles)

Dengvaxia- Dengue disease

Ervebo- Ebola

Collectively in consideration of transmission statements on package inserts, can government health agency representatives make statements about cases of a disease for which there is the possibility of transmission, as noted on various live-virus vaccine package inserts and CDC documents, without implicating a live-virus vaccine unless simultaneously disclosing to the public if the case was a wild-type or vaccine-type virus?

General research question: does the CDC only speak about vaccine-derived cases that occur in the public for polio because the live-polio vaccine is no longer used in the USA, and does this mean there will only be public disclosure of vaccine-derived cases in the future if and when licensing for other live virus vaccines is removed?

Research question: can the term ‘transmission’ extend from a 2nd person carrying a live virus to transmission to a 3rd person and beyond? If viruses replicate, and viruses can combine with other enteroviruses, then it should follow that transmission may or may not end with the person coming into contact with the person that received a live virus vaccine.

We return to the previously posed question: what is the logic of targeting low immunization rates for an “outbreak” or even a single case of a disease, when the origin of a case of a disease becomes obfuscated by live virus vaccines resulting in vaccine-derived cases?

Unless every single case is disclosed as either wild-type or vaccine-type, the public is left to assume whenever an emergency “outbreak” is declared that all cases are wild-type, which may not be the case when there’s a probability of transmission where transmission should only possible due to enough virus/bacterial replication.

Package Insert Statements on Adverse Events from Live-Vaccines: Can An Individual Contract the Disease itself from a Live-Vaccine?

“Not-Disease ≠ Disease,
Disease ≠ Disease-Probability,
Disease Probability = Disease / Disease + Not-Disease
therefore Not-Disease ≠ Disease because Disease ≠ Disease-Probability.
If Vaccine then Vaccine-Disease (aka Vaccine-Strain Case),
then Vaccine-Strain Case Probability from Vaccine,
because Vaccine-Disease Probability = Vaccine-Disease / Vaccine-Disease + Not-Vaccine Disease and because Not-Disease ≠ Disease” [24].

Per the CDC Pink Book, “When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease and is considered an adverse reaction to the vaccine. The immune response to a live, attenuated vaccine is virtually identical to that produced by a natural infection…” [28]

The CDC says an attenuated vaccine ‘does cause disease,’ therefore it can, which is not the same as ‘never’ thereby establishing a probability for an adverse event. In this case is “milder than the natural disease” is synonymous with “it is the disease itself from the vaccine” where ‘natural disease’ is interpreted as wild-type virus infection, where a vaccine contains an attenuated virus. The statement “usually much milder” also establishes a probability for mild ≠ not-mild, where there is a probability of cases not being mild.

“Not-Adverse Event ≠ Adverse Event,
Adverse Event ≠ Adverse Event-Probability,
Adverse Event-Probability = Adverse Event / Not-Adverse Event + Adverse Event,
therefore, Not-Adverse Event ≠ Adverse Event because Adverse Event ≠ Adverse Event-Probability.
If Vaccine then Vaccine Adverse Event-Probability,
then Adverse Event-Probability from Vaccine,
because Adverse Event-Probability = Adverse Event / Not-Adverse Event + Adverse Event and because Not-Adverse Event ≠ Adverse Event [23].”

In the official Maine of CDC statement regarding a case of measles, they state “it is not possible to contract measles from the vaccine.”

However, this contradicts the CDC Pink Book, “When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease and is considered an adverse reaction to the vaccine. The immune response to a live, attenuated vaccine is virtually identical to that produced by a natural infection…” [28]

Package inserts for various live-vaccines indicate in post-marketing sections the disease itself vaccinated against/for, and also include adverse events a “rash” from the disease, but “not” the disease apparently in spite of vaccinating with a live-virus/bacteria of the disease.

Some may argue that “Disease-like rash ≠ disease rash,” but this is incongruent with transmission statements where transmission of the disease should only be possible due to enough virus/bacteria replication (meaning a person has the disease from the moment of vaccination), and thus I hypothesize the following:
Disease(like)-rash = disease-rash -cancelling out disease-rash from both sides leaves…
Like = ? -what is the rash in likeness thereof? The only answer that makes sense is the disease itself. Like = Like Disease Vaccinated Against/For
which returns us to a correction where…
Disease-like rash = disease rash, where they do equal each other, even if ‘like’ is used to mean the ‘mildness’ of the vaccine-strain case, which is a probability to begin with as some cases are not mild as per CDC’s Pink Book statement that “When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease.” Usually = Probably, Probably = Probability, establishing a probability for non-mild cases.

In the package inserts below, it is unclear that scientific basis is used for calling a rash a disease-like rash, and not an actual rash from the disease. The term ‘like’ is a matter worth addressing in the context of 1. per CDC Pink Book statements on contracting the disease vaccinated against/for, and 2. transmission statements on vaccine package inserts.

Priorix- measles, mumps, rubella

MMR-II- measles, mumps, rubella

The statement “Testing to distinguish between rash caused by wild-type or vaccine virus was not performed,” is interpreted to mean the researchers most likely did not think it necessary to distinguish between wild-type virus and vaccine-virus in the sample considering reports of measles, rubella, and varicella were within 15 days of vaccination -why conduct tests to distinguish between wild viruses of those illnesses when patients had been given live viruses of those diseases via vaccines?

Hypothesized logical fallacy: how can the researchers call them “measles-like” rashes, “rubella-like” rashes, “varicella-like” rashes, and “mumps-like” rashes when the researchers declare there was no testing to distinguish between a rash caused by wild-type virus versus vaccine-viruses AND when there were 3 reports of actual measles, 1 report of actual rubella, and 1 report of actual varicella within 15 days of being vaccinated?

In other words: why are the rashes defined to be “-like” when actual attenuated viruses of those diseases are used in the vaccine?

Hypothesized correction: A weakened/attenuated virus of the disease is not “like” a virus of the disease; it’s a weakened virus of the disease. A weakened virus of a disease is not “like” a virus of the disease; it is the disease in weakened virus-form. Is a rash not a symptom of contracting the disease itself? How can one have a rash of a disease and not have the disease itself (albeit in weakened form)? How can there be an injection site rash of a disease without having the disease (in weakened form)? How can an individual be stated to have an immune response against a disease via an attenuated vaccine containing a live virus of a disease, yet not contract the disease itself (in weakened form) from the vaccine?

This is consistent with the previously discussed CDC definition of attenuated vaccines.

Research question: If vaccinating a patient with live attenuated viruses of measles, rubella, varicella, and mumps, how can the statement “the vaccine does not cause measles/rubella/varicella/mumps” be scientifically supported when rashes of those diseases can be a direct consequence of live-virus vaccine administration?

How can the CDC of Maine scientifically support the statement “it is not possible to contract measles from the vaccine” when rashes of measles can be a direct consequence of live-virus vaccine administration?

How can the CDC of Maine scientifically support the statement “it is not possible to contract measles from the vaccine” when the adverse reactions section of the MMR-II vaccine indicates it is possible for an individual to have an adverse reaction of atypical measles, measles inclusion body encephalitis, and “measles-like” rash -because how can a person have these specific adverse reactions in the absence of either wild-type measles or vaccine-virus?

What is the scientific basis for distinguishing a case of measles from a live virus measles vaccine from adverse reactions to a live-virus MMR-II vaccine that indicates atypical measles and measles inclusion body encephalitis when the vaccine insert indicates no testing was done to distinguish between wild-type of vaccine-type measles?

ProQuad (MMRV)- measles, mumps, rubella, varicella

In contrast to the MMR-II insert, the ProQuad package insert does not include statements regarding conducting testing to distinguish between wild type viruses and vaccine-viruses. It is not assumed such testing was conducted by omission of that statement considering similar Post-Marketing Experience adverse events and a similar statement regarding the definition of rashes being defined as “(disease)-like” rashes. If claims to having conducted such testing are made by a government health official or vaccine manufacturer representative, one can request that clinical data.

Previous questions regarding statements made by the CDC of Maine, hypothesized logical fallacies, and hypothesized corrections on the MMR-II vaccine are applicable to the ProQuad vaccine as well.

BCG (Live-Bacteria)

The BCG is a live-attenuated mycobacteria vaccine for treatment of bladder cancer and for prevention of bladder tumors.

Noted is the risk of BCG sepsis on the insert. Sepsis is defined on the CDC website: “Bacterial infections cause most cases of sepsis. Sepsis can also be a result of other infections, including viral infections, such as influenza. Fungal infections can also cause sepsis.”

ACAM2000- smallpox and monkeypox

‘Vaccinia’ is the name of the smallpox virus; thus, ‘Generalized Smallpox’ and ‘[Smallpox] Superinfection’ statements can be made, virus replication and virulence considered.

JYNNEOS

The postmarketing for this vaccine includes ‘rash,’ which could be indicative of a disease-rash from the vaccinia virus -an inactivated/non-replicating version of the virus used in this vaccine.

Vaxchora (Live-Bacteria)

As with the BCG vaccine, Vaxchora is also a bacterial vaccine.

How does the CDC distinguish between wild-type cholera from vaccine-derived cholera when vomiting and diarrhea are symptoms of both wild-type cholera yet also included in the adverse reactions section of the Vaxchora vaccine? Can the CDC make statements regarding vomiting or diarrhea as symptoms of cholera without implicating with live-bacteria Vaxchora vaccine in the greater context of transmission warning statements on the package insert, unless sequencing is done to ensure cases are wild-type?

Vivotif- Typhoid

Rash, stomach pain, fever, and diarrhea are indicated by the CDC as symptoms of typhoid, but also indicated as adverse events on the package insert for the Vivotif vaccine. If an individual is diagnosed with typhoid, how does the public know the case was wild-type or vaccine-strain to justify statements from public health agencies regarding so-called “outbreaks”?

Varivax- Varicella (chickenpox)

The package insert for Varivax indicates that during clinical trials testing to distinguish between wild-type and vaccine virus wasn’t performed.

How can the CDC make this definition when 1. the insert itself indicates testing to distinguish between wild-type or vaccine-virus wasn’t done in clinical trials most likely because the researchers assumed/knew it was vaccine-strain, and 2. when a person vaccinated with a live-virus can develop the same/similar rashes as varicella?

The post-marketing section of Varivax includes various statements on vaccine-strain varicella.

Since varicella-strain is also a component of the MMR-Varicella (MMRV) vaccine, the question is posed again: do we really understand chickenpox ‘outbreaks’ without virus strain sequencing data to ascertain exact numbers of wild-type or vaccine-strain cases?

RotaTeq- rotavirus

The package insert for rotavirus indicates gastroenteritus due to vaccine shedding in infants with or without immunodeficiencies. How can the vaccine both result in gastroenteritis and protect from rotavirus which per the CDC’s Pink Book the most common cause of gastroenteritis, and is this consistent with CDC Pink Book statements regarding a vaccine causing the disease vaccinated against/for?

Rotarix- rotavirus

Adenovirus

FluMist

YF-Vax -Yellow Fever

Dengvaxia- Dengue disease

‘Severe dengue infection’ post-vaccination supports CDC Pink Book statements for live-virus vaccines, establishing a probability for dengue infection from the vaccine.

Ervebo- Ebola

The adverse events from the vaccine and the symptoms of wild-type ebola per the CDC website appear to be clinically indistinguishable, as in the case of other live-vaccines as well and consistent with Pink Book statements.

Zostavax- Herpes Zoster (shingles)

The insert for Zostavax seemingly presents contradictory information, where the post-marketing section indicates infections with vaccine strain herpes zoster and vaccine strain varicella-zoster were reported, and yet the adverse events section states that that during clinical trials there were only 2 reports of the vaccine-strain.

Additionally, of the total 287 reported zoster-like or varicella-like rashes, the clinical trials used only 108 virus specimens for Polymerase Chain Reaction to determine wild-type versus vaccine-strain, leaving 179 rashes entirely untested.

Out of 287 cases of rashes, how is it possible to only have 2 reports of vaccine-strain related rashes?

Collectively, and in consistency with CDC Pink Book statements that live-vaccines can cause disease, the adverse events sections directly support assertions that an individual can contract the disease they are vaccinated against/for from the live-vaccine itself, and this is further grounded in transmission statements reviewed previously.

Are “Breakthrough Infections” Actually Vaccine-Strain Infections as per CDC Pink Book statements?

There is a term used in the literature referred to as a “Breakthrough” infection that presents itself ambiguously and warrants heavy scrutiny.

We’ve thus far reviewed CDC Pink Book statements that an individual can contract a disease they are vaccinated against/for, and these CDC statements are consistent with transmission and adverse events statements on vaccine package inserts discussed thus far.

The CDC Pink Book states, “To produce an immune response, live, attenuated vaccines must replicate in the vaccinated person. A relatively small dose of administered virus or bacteria replicates in the body and creates enough of the organism to stimulate an immune response. Although live, attenuated vaccines replicate, they usually do not cause disease such as that caused by the wild form of the organism. When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease and is considered an adverse reaction to the vaccine. The immune response to a live, attenuated vaccine is virtually identical to that produced by a natural infection because the immune system does not differentiate between an infection with a weakened vaccine virus and an infection with a wild virus” [28].

“Usually do not cause disease” ≠ “Never causes disease” because “Usually = Probability”
“Usually do not cause disease” = Vaccine-Disease Probability
“usually much milder” = non-mild Vaccine-Disease Probability
“When a live, attenuated vaccine does cause disease” = Vaccine-Disease-Probability

“A live, attenuated vaccine virus could theoretically revert to its original pathogenic form. This is known to happen only with live (oral) polio vaccine, which is no longer available in the United States” [28]. As stated previously and will be stated again, this CDC’s Pink Book statement is applicable to additional vaccines, where transmission is possible due to reversion to a pathogenic form, where the CDC’s definition of a ‘pathogen’ is an organism that causes disease, as well as consistency with CDC statements that ‘When a live, attenuated vaccine does cause disease, it is usually much milder than the natural disease.’

Breakthrough Infection = “Disease in spite of vaccination” per the CDC glossary, where ‘disease’ is ambiguously undefined on the CDC glossary, where each case of disease could be wild-type or vaccine-strain and requires analysis per case.

The CDC website defines ‘Breakthrough Varicella’ in a vaccinated person as being wild-type derived without genotype sequencing to rule out vaccine-strain despite being recently vaccinated.

How can the CDC make the statement that a “Breakthrough” infection of chickenpox after vaccination is absolutely wild-type when in clinical trials for various vaccines the package inserts direclty state no testing was conducted to distinguish between wild-type of vaccine-strain, as in the case of the aforementioned MMR and Varivax (varicella) vaccine?

Reminder: rubella-“like”, varicella-“like”, and mumps-“like” rashes were reactions found in clinical trials for the MMR-II vaccine as stated on the insert, with the pending research question that it should only be possible to have a rash from a disease if you have the disease -albeit perhaps and probable in mild form before considering non-mild cases, virus replication resulting in transmission, etc.

Above, the CDC defines a breakthrough infection as a measles infection in a vaccinated person without specifying whether it is wild-type or vaccine-strain, as per package insert distinguishing. “3 out of 100 people with 2 prior doses of MMR who are exposed to the virus…” -but what does ‘who are exposed to the virus’ mean? Does this mean exposed to wild-type virus after vaccination with vaccine-strain, or is this in regards to those who are exposed to the vaccine-strain virus?

Is human serology a red herring [False Cause] for studying breakthrough infections, when the definition of ‘breakthrough infection’ may be obfuscated by wild-type and vaccine-strain differences and the reacquiring of virulence of vaccine-strain viruses that may remain dormant after vaccination -as in the case of the ?

Research question: What is the scientific basis for studying immunological factors associated with ‘breakthrough infections’ without specifying, on a case-by-case basis, whether each breakthrough infection was wild-type or vaccine-strain? While above the CDC may state certain thresholds of HI antibody titers are associated with reduction in the risk of flu infection, this does not explain whether an infection occurred as a consequence of regaining virulence of a vaccine-strain, or a wild-type virus which carries initial implications prior to considering HI antibody titers due to the nature of vaccinating a person with a live-virus/bacteria vaccine which triggers antibodies in the first place.

In other words, how can antibody titers be used to study breakthrough infections after injecting a person with a virus/bacteria to trigger antibodies?

Hypothesized Logical Fallacies: Wicked Circle and False Cause, where antibodies are claimed to be needed to be studied to understand breakthrough infections (False Cause: hypothesized to be a False Cause because a person is injected with a virus/bacteria to trigger antibodies to begin with, so how can antibodies -the blamed False Cause- be examined to study wild-type-infection/breakthrough-infection/vaccine-strain-infection triggering the antibodies) thereby creating a Wicked Circle, and where breakthrough infections are ambiguously defined to create another False Cause and Wicked Circle (False Cause: wild-type or vaccine-strain infection should be understood first would be my hypothesis, because without this antibody titers become a False Cause, creating a Wicked Circle, where actual “cause” is ascertained to be infection itself as a consequence of wild-type or vaccine-strain viruses/bacteria).

If it is argued that the purpose of a live-vaccine is to prevent infection/transmission of wild-types via exposure to vaccine-strains and that this is why antibody titers are studied for breakthrough infections and other areas of research, the argument in itself has accepted the False Cause and Wicked Circle Fallacy; where a “breakthrough infection” is not properly defined as wild type via genetic sequencing to rule out vaccine strain (False Cause), and antibody titers are studied and blamed as being a factor impacting cases/outbreaks/breakthrough-infections (Wicked Circle).

In the previous section on the transmission statements for vaccine package inserts, I posited:

Based on CDC definitions:
Active(Immunity) ≠ Passive(Immunity), leaving…Active ≠ Passive
However, if Active means contracting a disease, and Passive means the passing of antibody protection…yet based upon polio literature it also means coming into contact with disease from vaccine-strain viruses being shed, then this turns into…
Active Immunity via wild-type virus/bacteria (contact with wild disease) = Passive Immunization (contact with disease via shedding) = Active Immunity (contact with live-vaccine disease)

How might this change our understanding of the CDC’s definition of a “Breakthrough Infection”?

Breakthrough Infection = “Disease in spite of vaccination” per the CDC glossary, where ‘disease’ is ambiguously undefined on the CDC glossary and each “disease” could be wild-type or vaccine-strain and requires analysis per case; therefore “Breakthrough Infection” = “wild-type or vaccine-strain infection” where the latter is determined by genetic sequencing and should not be scientifically assumed regardless of vaccination status, especially in light of arguments regarding lack of vaccination being a culprit for “Breakthrough Infections” that are poorly defined and lack genetic sequencing tests to begin with.

Thus, is a breakthrough infection a latent vaccine-strain infection/adverse event, as per CDC Pink Book statements that a person can get the disease they are vaccinated against/for, or is genetic sequencing available to confirm a wild-type case?

Is a Breakthrough Infection really just ‘Active Immunity’ via developing symptoms of the disease vaccinated against/for as per CDC definitions of live-vaccines, or is genetic sequencing available to confirm a wild-type case?

Is a Breakthrough Infection really just ‘Passive Immunity’ as per the polio literature definition regarding contact-transmission with another individuals vaccine-strain due to someone else’s vaccination and developing disease-symptoms despite being vaccinated, or is genetic sequencing available to confirm a wild-type case?

Collectively, vaccine package insert sections on rashes in likeness to the disease being vaccinated against/for, adverse events in likeness to symptoms of the disease, transmission statements, CDC Pink Book statements, and definitions of active versus passive immunity, warrant heavy scrutiny into exactly what the CDC defines as a “Breakthrough Infection.”

Death-reports on live-vaccine package insert, supporting CDC statements on a “remote chance” of vaccines causing “injury or death”

While the package inserts below may indicate comparable death rates between a vaccine group and a “placebo” group, worth remembering is that most placebos in vaccine clinical trials are not a saline-solution placebo, but a vaccine pseudo-placebo, which in reality may be interpreted as death data for two different sets of vaccines (e.g., imagine a researcher has one group eat chocolate cake everyday for a week and another group eat vanilla cake everyday for a week and measures differences in weight gain; can the researcher then conclude the benefits of eating chocolate and vanilla cake everyday outweigh the risk of weight gain if weight gain is linked to other adverse health outcomes?). This is also related to the topic of using sequelae after vaccination as an independent variable; when I first read Schultz et al. (2008), for example, I was surprised to learn the researchers did not use the MMR vaccine as the independent variable, but sequelae (rash, fever, diarrhea) after MMR vaccination to determine an association to autism risk [30]. Data is data, after all, and sequelae is data.

The lack of saline-solution clinical trials for vaccines has been the center focus of most vaccine-discourse, giving voice to vaccine-safety advocacy.

Death statements on vaccine inserts support the following equation:
Event ≠ Not-Event
Event = Vaccine(Death)
Not Event = not-Vaccine(Death)
Vaccine(Death) ≠ Vaccine(Death-Probability)
Vaccine(Death-Probability) = Events / Events + Not Events
…establishing the probability from the event.

Non-saline solution placebo controlled trials for vaccines support the following equation:
Vaccine(Death-Probability) ≠ alternative-Vaccine(Death-Probability)…
where significance tests are moot because mutually exclusive sets of data are obtained for separate vaccines.

ACAM2000

Research question: how can lack of vaccination be blamed -and thus greater vaccination targeted via marketing- for a death arising out of contact with an individual vaccinated with ACAM2000 when the insert states death has been reported in unvaccinated contacts “accidentally infected by individuals who have been vaccinated”? In other words, what is the logical basis for ruling a death as being due to “lack of vaccination” when an insert specifically states death has been reported due to contact/infection with those who have been vaccinated?

Research question: Since the insert indicates that deaths following ACAM2000 vaccination are “most often” the result of 1. cardiac death, 2. post-vaccinial encephalitis, 3. progressive vaccinia, or 4. eczema vaccinatum, and the insert also states that unvaccinated contact deaths have occurred due to accidental infection with ACAM2000 vaccinated individuals, are those four variables used as independent variables in the literature [and hospitals, autopsies to detect vaccine-strain, etc.] to rule out ACAM2000 vaccination as a factor impacting the death of an individual due to one of the four aforementioned variables?

BCG

Reminder- BCG sepsis is noted in the adverse events section of the insert, as was discussed previously.

RotaTeq- Rotavirus

Rotarix- rotavirus

Dengvaxia- Dengue disease

Vaxchora

What if an immunocompromised pregnant mother comes into contact with a vaccinated person shedding the virus from the vaccine?

MMR-II

Proquad

YF-Vax

Zostavax

Those who argue vaccines do not “cause” death or “result in” death, or state “there is no probability of death” after a vaccine, can address these statements on vaccine package inserts approved by the FDA.

Aforementioned is the CDC website statements for 26 vaccines regarding a “remote chance” of death.

Biological Hazards: Should OSHA and EPA regard and monitor Vaccine-Strain Transmission Cases as Biohazardous Events?

One major focus of OSHA and EPA guidelines regarding bloodborne pathogens centers around workplace safety against transmission of viruses.

The OSHA definition of bloodborne pathogens is inclusive of viruses; and the EPA’s definition of bloodborne pathogens does not limit the definition to solely HBV or HIV, as per Chapter 11 “Bloodborne Pathogen Exposure Control Plan” of their published 2024 Emergency Responder Health and Safety Manual.

Do EPA and OSHA definitions extend to live-vaccines with supporting evidence regarding adverse event-symptoms in likeness to the disease, rashes in likeness to the disease, transmission statements, confirmed genotype sequencing contact-transmission-vaccine-strain cases, and CDC Pink Book statements on live-vaccines?

Do OSHA definition implications extend to live-vaccines containing viruses/bacteria in spite of bloodborne pathogen guidelines focusing on the prevention of transmission of only specific viruses like HIV and Hepatitis B?

The NIOSH’s definition of biological hazards, while may be regarded by some as mutually exclusive from live-vaccines, by definition is actually mutually inclusive to the viruses/bacteria contained in live-vaccines for which there are transmission statements on package inserts.

The NIOSH’s definition of biological hazard is quite consistent with CDC vaccine glossary definitions of viruses, bacteria, pathogens, communicable, and infectious.

While some may regard viruses within vaccines as exclusive from the discussion of biological hazards, transmission statements on package inserts for live-vaccines, not to mention genotype sequencing tests that can confirm wild-type versus vaccine-strain, CDC Pink Book statements, etc., extend the implications of biological hazards to the live-viruses/bacteria in vaccines.

The disposal of waste regarded as biohazardous warrants awareness in light of CDC definitions of ‘virus,’ ‘bacteria,’ ‘vaccine,’ ‘live vaccine’ and ‘attenuated vaccine,’ and other definitions and their congruence with OSHA and EPA definitions.

Should the EPA exert a stronger influence and regard for live-vaccine transmission statements on package inserts, genotype sequencing that can confirm vaccine-strain transmission, present evidence regarding vaccine-derived polio, etc.?

Statements on various vaccine package inserts, although all vaccines require similar medical waste disposal, specify a biohazardous regard for the vaccine or other materials used in its administration.

BCG

“Because of the potential risk for transmission” is an important statement on this insert, where:

1. Implications can be extended to all live-vaccines using live viruses or bacteria
2. Transmission statements on inserts support the implication extension
3. Genotype sequencing to confirm contact-transmission vaccine-strain infections support the implication extension
4. A biohazardous-transmission event may or may not include contact with blood, as in the case of transmission statements where transmission can occur via contact with saliva or fecal matter
5. OSHA guidelines on preventing workplace exposure to infectious agents can be extended to live-vaccines
6. EPA guidelines on biohazardous waste and bloodborne pathogens can be extended to live-vaccines

YF-Vax

ACAM2000

The FDA-approved package insert for ACAM2000 indicates 1. a vaccine vial should be treated as biohazardous if its discolored or containing particulate matter, 2. Unused portions of ACAM2000 are treated as biohazardous, 3. excess droplets of vaccine and blood are discarded in a biohazard container, 4. the administration needle is discarded as a biohazard; 5. the Lyophilized Antigen Component, live vial, the stopper, the syringe and needle, the bifurcated needle, and gauze and cotton coming in contact with the vaccine are discarded as biohazardous; and 6. unused reconstituted ACAM2000 is discarded as biohazardous.

FluMist

The CDC’s 2007 “Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings” last updated in 2024 does warn against contact-transmission of bacteria and viruses [13].

Do these CDC definitions coincide with OSHA and EPA definitions of biohazards, where OSHA and EPA should monitor and regard vaccine-strain transmission of bacteria and viruses? Page 26 of the CDC guide certainly discusses vaccinia-virus transmission from vaccinated contacts; and yet transmission statements on additional live-vaccine package inserts, rashes in likeness to the disease vaccinated against/for using a live-vaccine, CDC Pink Book statements, etc. lend extension to the implication that OSHA and EPA should monitor and regard vaccine-strain transmission from live-vaccines. After all, the CDC’s own definitions are mutually inclusive with OSHA/EPA definitions.

New research questions based upon OSHA and EPA guidelines regarding biohazards and bloodborne pathogens, collectively combined with CDC definitions of vaccines, viruses, etc.:

• Should live-virus (attenuated) vaccines be labeled as a biological hazard?
• How can a live virus (attenuated) vaccine be marketed as “safe” while simultaneously meeting OSHA-EPA definitions for being a biological hazard?
• How can a live virus vaccine be marketed as “effective” while vaccine package inserts indicate a risk of live-virus/bacterial transmission due to containing a biohazard (a virus/bacteria)?
• Is fecal matter containing a live virus/bacteria a biohazard?
• Is wastewater and sewage containing live viruses/bacteria from vaccines due to shedding in the stool a biohazard?
• How should the published scientific literature and vaccine package inserts be updated for term usage of ‘biohazard’ as per EPA and OSHA definitions?

If it is argued that because a live-vaccine contains an attenuated/weakened virus and for this reason OSHA-EPA guidelines are not applicable to live-vaccines, the CDC’s own definition of a live-vaccine containing viruses/bacteria (e.g., they still contain live viruses/bacteria in spite of being in an attenuated form), as well as other definitions, should be regarded. Additionally, transmission statements on live-vaccine inserts, adverse events that are “a threat to human health” as per OSHA guidelines, rashes in likeness to the disease vaccinated against/for on package inserts, CDC Pink Book statements, etc. should be regarded. One may also regard current circumstances with the polio, where vaccine-derived polio, a threat to human health, the literature discussion of polio viruses reacquiring virulence after vaccination, and the CDC’s own involvement in worldwide recommendations on the use of live-polio vaccines, in considering transmission of live-viruses/bacteria as “threats to human health” and subject to substantial OSHA-EPA biological hazard pressure upon the CDC and the very science of vaccinology/virology.

If it is argued that live-vaccines prevent disease, and that is why OSHA-EPA guidelines regarding biological hazards are not applicable, then one can defer once again to evidence on vaccine package inserts regarding adverse events, rashes in likeness to the disease vaccinated against/for, CDC Pink Book statements that live-vaccines can sometimes cause the disease, transmission statements that contradict the foundation of so-called “disease-prevention” of vaccines (for how can a live-vaccine both prevent disease and result in disease via transmission), questionable “breakthrough infection” definitions without ascertaining wild-type versus vaccine-strain infections, etc.

Example Scenario 1: a 4 year old child receives a dose of MMR-II vaccine which contains 3 live viruses, unless it’s the MMRV which contains 4 live viruses. Although the assumption may be zero transmission cases, an assumption is a probability, especially in light of evidence reviewed thus far regarding transmission statements, CDC Pink Book, etc. etc. etc.; therefore, there may be live-virus transmission cases from that 4 year old to other children in the home setting and or daycare/school setting, leading to so-called “outbreaks.” Unless genotype sequencing is conducted on each case to ascertain wild-type versus vaccine-strain, officials of OSHA/EPA/NIOSH might believe that “outbreaks” were due to unvaccinated individuals coming into contact with wild-type strains, because 1. those representatives are not aware of aforementioned evidence on package inserts, the polio literature, transmission statements, CDC Pink Book statements, etc., and a literature does indicates outbreaks can occur among vaccinated populations. By OSHA/EPA/NIOSH definitions, a biohazard event occurred via such a live-virus transmission outbreak.

Example Scenario 2: the CDC-WHO involvement in worldwide polio vaccination has resulted in more cases of vaccine-strain polio than wild-type polio in various countries in recent years, and to the CDC and WHO’s credit, they appear to be forthcoming regarding genotype sequencing that confirms vaccine-strain cases for this virus literature alone -and less forthcoming regarding other live-vaccine vaccine-derived cases, as in the case of Maine that tested positive for vaccine-strain measles but the information was withheld from the public by the CDC until FOIA revealed the matter. By OSHA/EPA/NIOSH standards, the CDC-WHO actions have resulted in various biohazardous incidents, where the entire circulating vaccine-derived polio literature can be regarded as a biohazard impacting many countries. Vaccine-derived poliomyelitis can be life-threatening to the individual; and yet, somehow according to various organizations, lack of vaccination with live-vaccines, which may result in biohazardous transmission events of cVDPV in the first place, is the culprit…?

There’s a lot of contradictions in the foundations of vaccine-science, where definitions/understandings are regarded as mutually exclusive (e.g., a live-vaccine contains a live virus or bacteria, but it is not regarded as a biohazard by some individuals in spite of meeting definition criteria) with EPA-OSHA definitions of biological hazards when there is actually more inclusivity than there is not.

Per definitions, one distinction between OSHA’s bloodborne pathogens guideline is OSHA’s focus on transmission infection via contact with blood. This is inclusive but not exclusive from other modes of transmission (e.g., breast-milk, nose/throat, feces, etc.) indicated in the literature, where transmission of live-virus/bacteria need not occur through blood. Yet simultaneously, live-virus/bacteria presence in the blood due to live-vaccine vaccination arguably meets OSHA’s definition of a bloodborne pathogen.

Per CDC definitions:

Thus hypothesized the following linguistic correction:

“Live-(Virus/Bacteria)Vaccine = Biohazard“, because…

1. per CDC “virus = organism that causes disease“
2. per CDC “pathogens = organisms such as viruses/bacteria that cause disease”
3. per NIOSH “Biological hazards are disease producing agents (pathogens) that can be transmitted to individuals…
4. per CDC “communicable = that which can be transmitted“
5. per CDC “infectious = capable of spreading”
6. per vaccine inserts “transmission statements = communicable/infectious”
7. per CDC-WHO, vaccine-derived polio occurs due to transmission of live-viruses from vaccines, in some cases leading to vaccine-derived disease (poliomyelitis, and the literature regards it as indistinguishable from wild-type poliomyelitis)
8. per CDC Pink Book “When a live, attenuated vaccine does cause disease…”
9. in a previous section I hypothesized another linguistic correction:
   • “Disease-like rash = disease rash”, where they do equal each other, even if ‘like’ is used to mean the ‘mildness’ of the vaccine-strain case”
10. in a previous section I hypothesized that:
    • “breakthrough infection” = “vaccine-strain infection” and should not be assumed to be wild-type infection because sequencing is needed to differentiate wild-type from vaccine-strain in a recently vaccinated individual that received a live-virus/bacteria.

For reasons we shall delve into in a later section, OSHA/EPA/NIOSH may further regard live-vaccines as a biohazard as what is actually known about viruses for decades yields yet more troublesome questions upon the logic of the vaccine “science” foundations.

The NIH Virus Database without a Certain Little Datapoint

The NIH provides a database for viruses sequenced where an individual can filter for human hosts (homo sapien) and vaccine strain.

Considering this NIH database of viruses sequenced filtered for human hosts and vaccine strain, why is there only one measles data point in 2010 when internal CDC documents from 2023 confirm another human case of vaccine-strain measles -as was indicated on FOIA obtained documents regarding the case of Measles in Maine? [4] Why was the 2023 case of Measles that 2023 CDC documents confirm was ‘consistent with vaccine strain’ not added to this database?

Worth remembering is that the CDC boldly claims to be able to sequence over 7,000 flu viruses in a typical year.

Also worth remembering is that the WHO-CDC track vaccine-derived polio through genotype sequencing, and in 2022 the WHO published a strategy document for improving global surveillance tracking of viruses.

If this is the case, why does the NIH-NCBI Virus database yield less than 60 results when filtered for human hosts and vaccine strain, within the context of widespread live-vaccine use, rash-statements on inserts, no-testing for wild-type versus vaccine-strain statements on inserts, transmission statements, CDC documents warning against vaccinia transmission, the vaccine-derived polio-literature, etc.?

Wait…a Virus does WHAT in order to Replicate?

Genome.gov is an NIH website that explains the basic fundamentals of virus replication.

Research questions:

• If viruses are “genetic material,” how does this excuse lack of mutagenic/genotoxic potential safety tests for live-[genetic material] vaccines to ascertain the mutagenic/genotoxic impact of the injected live-[genetic-material] vaccine on the human-host?
• If viruses cause damage by “hijacking a host cell’s machinery to make copies of themselves” to disrupt normal cell function, how does this excuse lack of mutagenic/genotoxic potential Non-Clinical Toxicology safety tests for live-[genetic material] vaccines when a virus ‘disrupts normal cell function’ to begin with? [as well as within the greater context of package inserts for live-virus vaccines indicating transmission warnings, a vaccine-derived polio literature where the CDC and WHO themselves publish statements on efforts-struggles in the management of vaccine-derived polio “outbreaks”, internal CDC documents confirming ‘consistent with vaccine strain’ for a case of measles, etc.]
• If the NIH states viruses “cannot reproduce on their own. Instead, viruses replicate by infecting a host cell (such as humans, other animals, plants, or bacteria), hijacking the host’s biological machinery and turning the host cell into a virus-producing factory,” where are the published literatures on vaccine-derived cases for other live-[genetic material] vaccines since it is known viruses replicate by ‘turning the host cell into a virus-producing factory’ to begin with? [as well as within the greater context of package inserts for live-virus vaccines indicating transmission warnings, a vaccine-derived polio literature where the CDC and WHO themselves publish statements on efforts-struggles in the management of vaccine-derived polio “outbreaks”, internal CDC documents confirming ‘consistent with vaccine strain’ for a case of measles, etc.]

Research question: if in 1977 researchers sequenced the first viral genome, and as of September 2021 there were 11,465 viral genome sequences available, where are the other literatures on vaccine-strains infections other than polio?

Why does this NIH webpage make the statement that “previously” viral vaccines contained weakened or dead viruses when attenuated/weakened viruses are still used in the USA and around the world in 2026?

Why does the NIH website state viral vaccines are ‘incapable of causing disease,’ a contraction to vaccine package insert sections on adverse events, rashes, transmission, vaccine-strain infections, and CDC Pink Book statements?

Research Question: If “viruses that encode information with RNA rather than DNA tend to have a higher rate of mutations” and these mutations can happen in a human host as per previously reviewed statements by the CDC, WHO, and the vaccine-derived polio literature, where is the Non-Clinical Toxicology literature for live-[genetic material] vaccines evaluating the potential mutagenic/genotoxic effects of virus mutations as a consequence of live-[genetic material] administration?

Thus, basic statements on the NIH front page on genomics and virology lend implications regarding Non-Clinical Toxicology safety tests for vaccines regarding viral replication and cell damage; then again, if viruses didn’t cause cell damage, there wouldn’t be disease right?

My pending research questions as I dive deeper into the literature are:

• Can viruses result in genotoxic damage?
• What is the distinction, if there is one, between cell damage in a host due to a virus, and genotoxicity/carcinogenicity?
• How is cell damage related to carcinogenicity?
• How is cell damage related to genotoxicity?
• Is a disease from a virus a genotoxic/carcinogenic event?
• What is an adverse event, within the context of genotoxicity and cell damage?
• How is genotoxicity related to adverse events?
• What is the relation between virology, vaccinology, immunotoxicity, genotoxicity, and carcinogenicity?

Genotoxicity and Carcinogenicity of Viruses: Put them in the Ring- Virology versus…Vaccinology?

Virology seems contradictory to the field of vaccinology, where a deeper review of the virology literature supports assertions that virus infection can be genotoxic, and if viral infection is genotoxic then carcinogenisis can be the consequence.

The “safe and effective” narrative of vaccines contradicts the very foundations of virology that have been known for decades.

A widely cited 1996 university textbook available on the NIH website disucsses the potential chromosomal damage that may occur by viruses or indirectly via other means [40].

The 1996 year is significant for this paper, as 1996 is the first year HHS began providing industry guidance on genotoxicity evaluations of biological products, yet, as per this widely 1996 medical microbiology textbook, it was already known by 1996 that viral infection can be genotoxic.

Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Section 2, Virology. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8243/

“Genotoxic Effects: Following virus infection, breakage, fragmentation, rearrangement and/or changes in the number of chromosomes may occur” [40]. Autism Librarian notes– as early as 1996 it is known virus infection can be genotoxic; the year coincides with HHS recommendation for genotoxicity evaluation for biological products including vaccines.

“Chromosome damage may be caused directly by the virus particle or indirectly by events occurring during synthesis of new viral macromolecules (RNA, DNA, protein). The chromosome damage (Fig. 44-5) may or may not be faithfully repaired, and in either case, it may or may not be compatible with survival of the infected cell. When the cell survives, the virus genome may persist within the cell, possibly leading to continued instability of cellular genomic material or to altered expression of cellular genes (e.g., cellular oncogenes). Virus-induced genomic instability appears to be associated with accumulation of mutations and related to the process of cell immortalization and oncogenic transformation” [40]. Autism Librarian notes– the use of ‘immortalization’ term is interesting here in light of what are known as HeLa cells; is the implicit suggestion here that HeLa cells are the product of virus-induced genomic instability?

“Shedding of Virus: Although the respiratory tract, alimentary tract, urogenital tract and blood are the most frequent sites of shedding, diverse viruses may be shed at virtually every site” [41]. Autism Librarian notes– implication-extension for shedding statements on live-vaccines, as well as OSHA/EPA/NIOSH guidelines for protecting the public from infectious diseases.

“Disease does not always follow successful virus replication in the target organ. Disease occurs only if the virus replicates sufficiently to damage essential cells directly, to cause the release of toxic substances from infected tissues, to damage cellular genes or to damage organ function indirectly as a result of the host immune response to the presence of virus antigens” [41]. Autism Librarian notes– implication-extension to adverse events, including post-marketing adverse event reports.

“Host immunosuppression is often associated with reactivation of a number of persistent virus infections” [42]. Autism Librarian notes– implication-extension to dormant viruses, where vaccination with a live-vaccine introduces a virus that may become dormant due to case-by-case reasons, later reactivated.

“Viral replication is influenced strongly by temperature. … Artificial induction of fever reduces mortality in mice infected with viruses. Artificial lowering of the temperature during infection may increase mortality, as in suckling mice infected with coxsackieviruses and taken away from the warmth of their mother’s nest. Fever also augments the generation o cytotoxic T lymphocytes” [43]. Autism Librarian notes- are there implications for modern air-conditioning or fever-reducing medications such as acetaminophen? If acetaminophen interferes with fever-induced by viral infection, is acetaminophen then interfering with a reduction in viral replication in the host? This could place the acetaminophen in an interesting position regarding association with autism, where a lone association without virus-exposure in a pregnant mother is one independent variable (already supported in the acetaminophen animal literature), but association via virus replication-noninhibition due to fever-suppression impacting virus replication (which undoes ‘confounding by indication’ arguments for acetaminophen or other fever-reducing products) is supported where maternal immune activation and early life infection is associated with an increased risk of autism and viral-replication via acetaminophen or other drugs (immune activation). In other words, if the body’s rise in temperature is supposed to inhibit viral replication, and immune activation is associated with increased risk of autism (whether it’s maternal immune activation during pregnancy or early life infections in the offspring), then I would hypothesize that a fever-reducing medication that interferes with the inhibition of viral replication from the fever places that medication into a relationship with viral replication and immune response, and derivative relations. What other variables exist that fit into definition of ‘artificial lowering of the temperature’ that should be considered in this literature?

“Also consistent with these findings is the observation that virus strains that replicate best at fever temperature are usually virulent, whereas virus strains that replicate poorly at fever temperature are usually low in virulence and therefore often are used as live virus vaccines” [43]. Autism Librarian notes– the assumption, then, would be that a live-virus vaccine triggers a fever; implication then, is that if there is no fever or a certain threshold of “fever” is not reached to negatively impact virus replication in the vaccinated person, the virus strain can replicate more freely. What factors impact a case reaching “fever” threshold needed for their own body to reduce/negatively-impact viral replication? But then, what is vaccine-failure, if there is not enough replication to stimulate an immune response? Contraindication of antivirals and antibody-containing blood products for the timing of vaccine administration is also worth noting here because they would interfere with virus replication (e.g., in a previous section, we discussed how the ProQuad insert specifically contraindicates immune globulins because they interfere with virus replication; a CDC page on contraindications mentions antivirals and antibody-containing products for specific vaccines, although they do not specifically state interference with replication, but do also mention antibacterial drugs interfering with the live-typhoid vaccine). Is this a Wicked Circle, where virus replication is the “cause” of disease, yet per aforementioned contraindications virus replication should not be inhibited?

“This complexity arises from the many components of the host immune defenses and their interactions with one another. The existence of a variety of defenses is not surprising in view of the diversity of viruses, hosts, routes of infection, body compartments, cells, and mechanisms of virus multiplication and spread. The situation is further complicated by the varying effectiveness of the different host defenses during the different phases of the primary viral infection (implantation, spread to target organs, and subsequent recovery of each of the infected tissues), as well as during resistance to reinfection. Furthermore, the activated host defenses can actually cause disease manifestations” [43]. Autism Librarian notes– implications for Post-Marketing immune system disorders, rash statements, vaccine-strain infections, and “breakthrough infections.”

“At least three immunoglobulin classes have been demonstrated to exert antiviral activity: IgG, IgM, and IgA. These antibodies can neutralize the infectivity of virtually all known viruses. Antibody binds to the virus extracellularly, either neutralizing it immediately or blocking its interaction with host cells. Antibody that has bound to virus can block the infection of a cell at one of three steps: (1) attachment of virus to the cell surface, (2) penetration of virus into the cell, and (3) uncoating of virus inside the cell (Fig. 50-3). The mechanism of viral neutralization involves the binding of antibody to virus coat proteins; this usually alters the viral receptor for the target cell. More rarely, bound antibody may also interfere with penetration or uncoating” [43]. Autism Librarian notes– CDC contraindicates antibody-containing blood products 11 months or less prior to MMR and Varicella vaccination, which per this textbook is because it would block cell infection. Erego, cell infection needed to stimulate an immune response; yet cell infection is synonymous with the replicating nature of a virus that damages host cells in order to replicate, then cell damage due to a virus is what stimulates an immune response, because cell infection involves cell damage.

The books “Principles of Virology” Volumes 1 and 2 by Flint et al. (2020) provides further insights into viruses/bacteria invasion process where cell damage is part and parcel of their infection and replication processes, often resulting in genotoxic damage.

Genotoxic damage from viruses/bacteria-

“Vaccines Save Lives” Continues to be Separate from Non-Clinical Toxicology: Let’s Get Into Specifics…

Logical bases:

• An adverse event to a vaccine may be considered a genetic reaction (i.e., genes are not separate from health, they are one and the same). In this regard, Non-Clinical Toxicology is related to the adverse events literature and Vax-Unvax studies.
• An adverse event does not indicate when, how, under what circumstances, or even if complete genetic repair occurs after a minor adverse event (e.g., a person may recover from an adverse event insofar as symptoms are concerned, but there may be lingering unrepaired genetic damage).
  • In this regard, vaccine package inserts, which may indicate recovery after adverse events, do not cover any remaining potential undetectable genetic damage.
• Vaccine administration, whether single, multiple, and cumulative, may not result in a detectable adverse event, although genetic damage may still occur. For this reason, I previously stated Non-Clinical Toxicology was separate from other literatures.
• Thus, the adverse events literature of vaccines, including Vax-Unvax literature, is:
  • 1. un-separate from Non-Clinical Toxicology in that adverse events may assist in designing Non-Clinical Toxicology research for genes associated with the adverse events, illnesses, etc. linked to vaccine administration, because an adverse event or an illness as a consequence of vaccines is a genetic reaction/outcome.
  • 2. separate from Non-Clinical Toxicology in that adverse events do not cover undetected genetic damage that may not result in a detectable adverse event/illness or that is un-linked to the adverse event/health outcome that was detected/diagnosed (i.e., genetic damage resulting in increased risk of Bells Palsy that did not result in an initial adverse event; as another example, undetected genetic damage in addition to Bell’s Palsy impacting risk of an alternative disease).
    • Sub question: wouldn’t the detection of the Bell’s Palsy due to a vaccine cover the genetic portion of Non-Clinical Toxicology to just bring us back to Vaccinated versus Un-Vaccinated studies and those differences in health outcomes?
      
      Argued ‘no’ because the parameter is actual diagnosis of Bell’s Palsy or another disease, which is less conservative than the genetic markers that may or may not result in Bell’s Palsy or another disease. That’s what Non-Clinical Toxicology provides, a more conservative approach prior to formal diagnosis or in spite of a diagnosis that may presume no other genetic damage (e.g., the limiting parameters of formal diagnosis).
      
      Non-Clinical Toxicology basically can take things much further.
      
      The ‘may or may not’ of genetic damage and repair that ‘may or may not’ result in a parametered-diagnosis is the factor that separates Non-Clinical Toxicology from the other literatures, in that Non-Clinical Toxicology research may be able to detect genetic mutations prior to genetic repair for whatever factors that influence genetic repair and hide genetic damage from vaccines).
      
      Do we know if excellent nutrition, exercise, etc. ameliorate any potential genetic damage from vaccines?
      No. That research doesn’t exist.
      
      Do we know if certain people have genetic predisposition for genetic repair to ameliorate any potential genetic damage from vaccines? No. That research doesn’t exist.
• Research question: is the follow up of vaccine clinical trials, or the post-approval research as noted in the post-marketing experience sections of vaccine package inserts, any picture of mutagenic/carcinogenic potential of vaccines within the contest of Non-Clinical Toxicology?
  
  Argued ‘no’ or ‘partially,’ since 1. Non-Clinical Toxicology safety tests would need to be conducted with follow up periods that at a bare minimum cover the entire childhood “schedule,” and (and as this library is concerned, emphasis on genetic mutations impacting increased autism risk in the offspring or in the parents passing on mutations impacting autism risk in their offspring) 2. adverse events covered by the current literature most likely do not encompass undetected genetic damage from single, multiple, or cumulative doses of vaccines that don’t result in formal diagnoses of illnesses.
  
  The adverse events literature including Vax-Unvax studies are useful to “reverse engineer” those genetics studies. How do we know that while a vaccine(s) may be linked to an adverse health outcome (e.g., encephalopathy), the genetic consequences of that adverse health outcome may be linked to other health outcomes (e.g., autism) traced back to the genetic damage from the vaccine(s) itself that resulted in the initial adverse health outcome (encephalopathy)?

Biological Products, the Virus-Toxin Law, and ‘Genetic Material’ used in Viral Vaccine Production

Government health agencies consider vaccines to be a biological product, and the 2023 Guidance for Industry from the Department of HHS states that the assessment of the mutagenic potential is not for biological/biotechnological products. This first occurred in 2006, when HHS stopped recommending mutagenic safety tests for biological products a decade after first recommending them in 1996.

Exactly how and when did vaccines earn the label of a ‘biological product’?

A 2018 FDA publication titled “Science and the Regulation of Biological Products” references the growing of viruses in tissue culture for the development of the polio vaccine, the preparation of a weakened live-[virus] vaccine for German measles (rubella), and the use of bacteria for the creation of the pertussis vaccine. The Biologics Control Act of 1902 was passed to ensure the safety of biological products, and the FDA’s Center for Biologics Evaluation and Research (CBER) is responsible for regulating “biologics.”

The FDA states in regards to the Biologics Control Act of 1902:

“This law was enacted by Congress to ensure the protection of Americans by providing consistently safe biological products. The Act not only serves as the underpinning for today’s regulation of biological products, but also marks a historic turning point in the way America protects the health of its citizens.”

Center for Biologics Evaluation and Research (CBER)- “CBER is responsible for the regulation of “biologics,” which are medical products such as vaccines, blood and blood derivatives, allergenic patch tests and extracts, HIV and hepatitis tests, gene therapy products, cells and tissues for transplantation, and new treatments for cancers, arthritis, and other serious diseases. CBER reviewed the first vaccines to immunize persons against infectious diseases, such as polio, pertussis (“whooping cough”), and German measles.”

“In 1901, diphtheria patients were routinely treated with antitoxin derived from the blood serum of horses. The horse serum was manufactured in local establishments with no central or uniform controls. In St. Louis, Missouri, the blood of a tetanus-infected retired milk wagon horse named Jim was used for that purpose. By late 1901, this situation erupted into tragedy when 13 children who had been given diphtheria antitoxin died of tetanus. In 1902, Congress enacted the Biologics Control Act, also known as the Virus-Toxin Law, which gave the government its first control over the processes used for the production of biological products. The first regulations under this Act became effective on August 21, 1903, and mandated that producers of vaccines be licensed annually for the manufacture and sale of vaccines, serum, and antitoxins.”

Thus, the Virus-Toxin Law came to be due to a contamination of a treatment for diphtheria derived from the genetic material of a horse.

What other historical contamination is acknowledged by the CDC?

Above, the CDC states that there was found no causal association between receipt of the SV40-contaminated polio vaccines and cancer. However, a review of the 9 CDC citations indicates that the statement was not based on Non-Clinical Toxicology safety tests on the contaminated vaccines. What would such safety tests have revealed?

Is isolated SV40 detection and use as an independent variable equivalent to the use of the entire contaminated vaccine in Non-Clinical Toxicology safety tests for a polio vaccine, which worth noting may contain other live polio strains of viruses if not the IPV vaccine, in regards to conclusions purported to have external validity as concerns Non-Clinical Toxicology?

What would Non-Clinical Toxicology safety tests reveal about the Rotarix and RotaTeq contaminated with live-PCV?

Is isolated PCV detection and use as an independent variable equivalent to the use of the entire contaminated vaccine containing a live virus in regards to conclusions purported to have external validity as concerns Non-Clinical Toxicology?

What other material is used to manufacture a viral vaccine?

Above the FDA indicates that there is fetal calf/bovine serum in some vaccines.

However, why is only calf/bovine serum included on this FDA page when other vaccines use human cells, porcine cells, and monkey kidney cells to grow a virus and the FDA directly provides guidance on the use of such cells?

A 2010 FDA Guidance document titled “Characterization and Qualification of
Cell Substrates and Other Biological Materials Used in the Production of Viral Vaccines for Infectious Disease Indications,” the latest guidance document on these matters:

“We, FDA, are providing you, manufacturers of viral vaccines, guidance for the characterization and qualification of cell substrates, viral seeds, and other biological materials used for the production of viral vaccines for human use.” (pg 1)

“The regulations, in 21 CFR 610.13, state in part that “Products shall be free of extraneous material except that which is unavoidable in the manufacturing process described in the approved biologics license application.” In 21 CFR 600.3(r), purity is defined as the “relative freedom from extraneous matter in the finished product, whether or not harmful to the recipient or deleterious to the product.” (pg. 3)

“Live attenuated viruses, whole inactivated virions, or virus-like particles often cannot be purified as rigorously as viral subunit vaccines; as a consequence, the potential for contamination is greater than that of subunit vaccines.” (pg. 3)

“For inactivated vaccines, the concern is that the process used to inactivate the vaccine virus may not inactivate all adventitious agents potentially present (as occurred with early inactivated poliovirus vaccines [Ref. 4]). Therefore, you should validate your process for inactivation of adventitious agents using different model viruses (Ref. 2).” (pg. 3)

“If you are using primary monkey kidney cell cultures, for example, you should test for species-specific simian agents, such as SV40 and herpes B virus, and other simian agents, such as simian polyomaviruses and simian cytomegalovirus.” (pg. 11)

“For example, if adenovirus sequences are used to transform a primary human cell to produce a cell line (e.g., 293 cells), then testing should demonstrate that the final product is free of the introduced viral sequences. Similarly, if a virus is used to transform cells, that virus and its genetic material should not be detectable in the final product using an assay with sensitivity sufficient to provide assurance of safety.” (pg. 14)

“Bovine serum should be free of adventitious agents, including bacterial and fungal agents, mycoplasmas, mycobacteria, and bovine viruses (Section IV.A.2.f).” (pg. 17)

“Cultures must be tested for the presence of detectable microbial agents and tests necessary to assure the safety and purity of the product may be required (21 CFR 610.18). Your biological starting materials should be characterized sufficiently to ensure that they do not contaminate the final product with
extraneous infectious organisms, such as bacteria, fungi, cultivatable and non-cultivatable mycoplasmas and spiroplasma, mycobacteria, viruses, and the agent(s) responsible for transmissible spongiform encephalopathies (TSEs). For a substance to be considered free of a contaminant, your assay should demonstrate, at a predefined level of sensitivity, that a certain quantity of the substance is free of that contaminant. Alternatively, a validated process that is known to remove a contaminant to a defined level may be used to demonstrate the absence of that contaminant. If an adventitious agent is known to be present in your cell substrate or viral seed, then you should demonstrate that your production process is sufficiently robust to eliminate or inactivate the agent with an appropriate margin of safety.” (pgs. 19-20)

Human diploid cells and monkey kidney cells are commonly used and are
often susceptible to infection by many of the viruses listed below. Specialized
cell culture testing might be needed to detect growth of other viruses. For
example, in vitro adventitious agent testing of insect cells should be capable
of detecting different families of insect viruses that could infect the host from which the cell substrate was derived. This should also include a cell line
broadly susceptible to arboviruses, such as BHK21. (pg. 24)

“If the possibility of contamination with human or simian cytomegaloviruses is a consideration, the first set of human cell cultures should be observed for at least 4 weeks unless a shorter incubation period is shown to be equally sensitive.” (pg. 25)

You should source bovine-derived reagents in a manner that minimizes the risk of contamination from BSE (Ref. 33). We recommend that you consult with CBER for more information. In some cases, a BSE risk assessment can address BSE-related issues. We recommend that you test bovine-derived reagents using assays…” (pg. 28)

“Testing of porcine-derived reagents for these agents is an important component of providing this assurance. Under certain circumstances, additional tests might be needed. Agents of concern from porcine cells listed in 9 CFR 113.47(b)(1) and (6) include: porcine parvovirus, bovine viral diarrhea virus (BVDV), reovirus, rabies virus, porcine adenovirus, transmissible gastroenteritis virus (TGE), and porcine hemagglutinating encephalitis virus.” (pg. 29)

At least 9 out of 10 animals injected with positive control cells (e.g., HeLa cells or other cells with comparable tumorigenicity) should show progressively growing tumors in order for your test to be valid. (pg. 34)

“For example, immortalization of primary cells with viral oncogenes to generate a complementing cell line for production of defective viruses or viral vectors will inevitably change the phenotype of the cell. Such manipulations might induce the expression of latent or endogenous viruses, and/or might cause the cells to become tumorigenic.” (pg. 12)

The here FDA states “Products shall be free of extraneous material except that which is unavoidable in the manufacturing process described in the approved biologics license application.” In 21 CFR 600.3(r), purity is defined as the “relative freedom from extraneous matter in the finished product, whether or not harmful to the recipient or deleterious to the product.”

How can a vaccine be marketed as ‘safe’ if the FDA states a definition of purity includes “whether or not harmful to the recipient” and how can a vaccine be marketed as ‘effective’ if the FDA definition of purity includes “deleterious to the product”?

The FDA’s definition of the ‘purity’ of a vaccine yields implications for Non-Clinical Toxicology” insofar as:

1. Less-contaminated vaccine effects on genotoxicity/carcinogenicity
2. More-contaminated vaccine effects on genotoxicity/carcinogenicity;
3. Multiple-dose vaccine doses, degree of contamination considered, effects on genotoxicity/carcinogenicity
4. Cumulative-dose vaccine doses, degree of contamination considered, effects on genotoxicity/carcinogenicity.

Research question: how does virus/bacterial contamination effect genotoxicity/carcinogenicity via potential recombining with other viruses/bacteria, whether live-viruses/bacteria in a vaccine, latent/dormant viruses/bacteria in a person, or due to multiple-dose administrations in a single visit?

[Section to be updated after my further review of virology literature]

Non-Clinical Toxicology: Vaccinated Versus Un-Vaccinated Studies, and Future Horizons for Genetics Literatures

Vaccinated-Unvaccinated studies provide valuable information regarding the link between vaccines and formal diagnoses of illnesses. However, they may not provide a complete analysis of genetic harm that may or may not be reflected in adverse events and formal diagnoses due to the very nature of genetics -a genetic predisposition for a disease does not mean one will develop the disease, which is why healthy lifestyle recommendations are so paramount to longevity. Thus, Vax-Unvax studies may not be providing a complete picture due to 1. missed diagnosis, 2. errors in diagnoses, 3., no formal diagnosis of a disease in spite of genetic predisposition for the disease.

A conservative approach to the research literature will look at mutagenic effects of vaccines impacting genetic predisposition for illnesses by looking at genes impacting diseases independent of diagnoses/failure to diagnose those diseases (i.e., Vax-Unvax studies).

Nevertheless, vaccinated and unvaccinated studies can provide a “map” of where research direction should be headed for a vaccine-genetics literature. The CDC’s Vaccine Safety Datalink can provide valuable data in its ability to analyze the link between vaccination and the development of illnesses over much longer periods of time than vaccine clinical trials used to approve a vaccine. One can then use that data to “reverse-engineer” studies to look at the genetic impact of vaccines and those illnesses found to have a direct link to higher vaccination rates. The CDC’s Vaccine Safety Datalink’s worth is in pushing forward a vaccine-genetics literature to provide the basis for funding such research.

As it concerns other drugs/products on the market without mutagenic and carcinogenic potential safety tests, a similar database is needed to 1. determine links between a drug and the risk of a health outcome, in order to 2. “reverse engineer” drug-genetics research to examine genetic/carcinogenic harm arising out of the drug (e.g., Non-Clinical Toxicology drug-drug interactions should be its own separate literature and perhaps a separate section on package inserts).

The database would provide the basis for funding drug-genetics research to populate all of the missing Non-Clinical Toxicology sections of inserts -and would be a great area of study for genetics researchers wishing to un-confound their findings. As it stands, no genetics literature is without confounding by the presence of pharmaceuticals with absent Non-Clinical Toxicology sections on package inserts.

Extremely concerning, and with serious implications, is the treatment of any disease with a product that was never tested for mutagenic and carcinogenic potential for a disease whose origin is confounded by the presence of products in the market that never underwent mutagenic/carcinogenic potential safety tests.

This is presently happening with Wellcovorin, where Non-Clinical Toxicology sections of package inserts indicate the drug has never been evaluated for mutagenic/carcinogenic potential, and yet the drug is marketed by the FDA to treat a genetic disorder.

References

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2. Autism Librarian (2026, January 19). Non-Clinical Toxicology Spotlight: 9 Simple Ways This Overlooked Section on Package Inserts Changes Vaccine Discourse. https://thecausesofautism.com/2026/01/19/non-clinical-toxicology-spotlight-9-simple-ways-this-overlooked-section-on-package-inserts-changes-vaccine-discourse/
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18. Open VAERS. Vaccine Excipients. https://openvaers.com/resources/vaccine-excipients

I believe Open-VAERS began their project of listing every vaccine package insert available because they were not previously available on the FDA website and it’s one of the reasons I listed them as a source on the main vaccine page of this library. Incidentally, it was through reviewing various vaccine package inserts and extracting post-marketing adverse events sections onto the main vaccine page in this library (specifically looking for encephalopathy) that I kept seeing the Non-Clinical Toxicology sections of package inserts, leading to my subsequent publications on the matter. However, through my course of researching this article I came upon an FDA page that lists all package inserts for vaccines currently licensed extending beyond what OpenVAERS has available. Because live-polio vaccines are not licensed in the USA in spite of their use in other countries, they are unlisted. The same is true for other vaccines that may be licensed in other countries. Thanks to this (new?) FDA page, I’m able to update the Non-Clinical Toxicology mindmap with the following vaccine inserts: Cyfendus (Anthrax), Vimkunya (Chingunkunya), Prehevbrio (Hep B), Cervarix (HPV),

VAERS-HHS

“VAERS reports alone cannot be used to determine if a vaccine caused or contributed to an adverse event or illness.”

“The number of reports alone cannot be interpreted as evidence of a causal association between a vaccine and an adverse event, or as evidence about the existence, severity, frequency, or rates of problems associated with vaccines.”

It is unclear why data provided to HHS, why a person reporting their own or another person’s adverse reaction to an event, appears to be undermined or rejected as 1. an event, or 2. establishing a probability for an event when the VAERS was was created for the very reason or providing data-events.

I publicly discussed this on X in early 2025 when I was working on the Acetaminophen literature review when I found one study that did use sequelae as an independent variable.