BEFORE 2020, very few members of the public knew the meaning of the term “disease enhancement”. After 2020, it has become widely understood that coronavirus vaccines have, in the past, caused worse health outcomes upon viral infection.
The rush toward vaccinations against SARS-CoV-2 had skipped early animal studies.
Therefore, I sent the following message to ACIP, the committee that chooses whether any vaccine and which vaccines are recommended for children, and more recently, for adults.
The animal studies conducted in the past on MERS and SARS vaccines show unequivocally that vaccines against members of this clade of coronaviruses caused DISEASE ENHANCEMENT, mostly in the older animals, meaning more severe COVID upon exposure to the virus following vaccines. The two studies conducted by Moderna and Pfizer on the leading vaccines failed to measure for enhanced immunopathology in any organ site other than the lung – and they failed to measure a key indicator of disease enhancement (IL-5). Pfizer removed an outlier from their small study, which is not accepted practice in the statistical analysis of studies such as these.
My own research shows that all immunogenic epitopes in the SARS-CoV-2 virus except one have high potential for pathogenic priming due to homology to human proteins in a wide variety of human tissues (Lyons-Weiler, 2020). Since no animal studies were conducted on older animals, we have no idea of the COVID19 vaccines being considered will cause pathogenic priming leading to disease enhancement in the liver, pancreas, spleen, brain, intestines, and central nervous system. Unqualified recommendations of COVID19 vaccines could lead to a public health crisis due to disease enhancement that makes 2020 look like a walk in the park.
The vaccine should be sent back to the drawing board for proper translational studies. Unsafe epitopes should be removed. I have peer reviewed three COVID19 vaccine studies and the authors of those studies all agreed to remove the unsafe epitope found easily by computational search.
I urge with every ounce of my scientific background that you specifically exclude the elderly from recommendation until autoimmune and immune reactogenicity is fully studied in older animals. Further, given the head-spinning pace at which the vaccine studies have been conducted, especially given the combination of Phase2/3, the lack of screening for prior exposure, the dubious interpretations of efficacy published in press-releases without rigorous peer-review, I strongly recommend that you caveat any recommendation of COVID19 vaccines for any population “without mandate” and similarly for any future and past ACIP-recommended vaccine. This at the very least would help stop any insurrection or rioting that will occur if millions of people experience more serious COVID19 symptoms or mass deaths following infection following vaccination.
I attach my NIH Biosketch so that you might consider some of my peer-reviewed research studies in your deliberations.
I also provide references to the studies cited below.
Some contextual comments: I and millions of our fellow Americans have grave concerns regarding testing false positive rates (see Lee, SH. Testing for SARS-CoV-2 in cellular components by routine nested RT-PCR followed by DNA sequencing. International Journal of Geriatrics and Rehabilitation 2020, 2(1):69- 96 and Basile K et al., Accuracy amidst ambiguity: false positive SARS-CoV-2 nucleic acid tests when COVID-19 prevalence is low, Pathology, 2020 https://doi.org/10.1016/j.pathol.2020.09.009) as well as grave concerns over the change in the practice of the diagnosis of COVID19 using only qRT-PCR results of which the entire committee should also become aware (e.g., Ealy, H, M McEvoy, D Chong, J Nowicki, M Sava, S Gupta, D White, J Jordan, D Simon and P Anderson. COVID-19 Data Collection, Comorbidity & Federal Law: A Historical Retrospective. Science, Public Health Policy & the Law Oct 2020 2:4-22.).
Since early treatment with any number of published therapeutic protocols can reduce the incidence of serious illness and mortality from COVID19, I urge ACIP to recommend early and prophylatic use of hydroxychloroquine, budesonide. See http://c19study.com/ for a compilation of studies that support early use of hydroxychloroquine.
You and all who serve in public health are just that – public health servants. You are not an elected board, you should not be empowered with the de facto power of rule of law by decree. That type of law-making was rigorously ousted from these United States of America in 1776. I ask on behalf of all who will suffer lifelong chronic illness and death from a COVID19 vaccine mandate – please do your job and provide proper stewardship of all aspects of public health. Respect choice.
Sincerely,
James Lyons-Weiler, PhD
Pittsburgh, PA
Lyons-Weiler J. 2020. Pathogenic Priming Likely Contributes to Serious and Critical Illness and Mortality in COVID-19 via Autoimmunity. J Transl Autoimmun. 2020 Apr 9:100051. doi: 10.1016/j.jtauto.2020.100051.
Immunization with inactivated Middle East Respiratory Syndrome coronavirus vaccine leads to lung immunopathology on challenge with live virus. “Lung mononuclear infiltrates occurred in all groups after virus challenge but with increased infiltrates that contained eosinophils and increases in the eosinophil promoting IL-5 and IL-13 cytokines only in the vaccine groups. Inactivated MERS-CoV vaccine appears to carry a hypersensitive-type lung pathology risk from MERS-CoV infection that is similar to that found with inactivated SARS-CoV vaccines from SARS-CoV infection.” https://www.ncbi.nlm.nih.gov/pubmed/27269431
Vaccine efficacy in senescent mice challenged with recombinant SARS-CoV bearing epidemic and zoonotic spike variants.“VRP-N vaccines not only failed to protect from homologous or heterologous challenge, but resulted in enhanced immunopathology with eosinophilic infiltrates within the lungs of SARS-CoV-challenged mice. VRP-N-induced pathology presented at day 4, peaked around day 7, and persisted through day 14, and was likely mediated by cellular immune responses.” https://www.ncbi.nlm.nih.gov/pubmed/17194199
Immunization with Modified Vaccinia Virus Ankara-Based Recombinant Vaccine against Severe Acute Respiratory Syndrome Is Associated with Enhanced Hepatitis in Ferrets “Immunized ferrets developed a more rapid and vigorous neutralizing antibody response than control animals after challenge with SARS-CoV; however, they also exhibited strong inflammatory responses in liver tissue.”
https://jvi.asm.org/content/78/22/12672.abstract
Animal Models for SARS and MERS coronaviruses. “The concern that is extrapolated from the FIPV vaccine experience to human SARS-CoV vaccines is whether vaccine recipients will develop more severe disease if they are exposed to or infected with SARS-CoV after neutralizing antibody titers decline. The second concern is whether recipients of a SARSCoV vaccine would be at risk of developing pulmonary immunopathology following infection with an unrelated human coronavirus e.g. 229E, OC43, HKU1 or NL63 that usually causes mild, self limited disease. Although findings from preclinical evaluation have revealed these concerns, studies in animal models may not be able to provide data to confirm or allay these concerns.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550498
https://science.sciencemag.org/content/303/5660/944.ful
Thank you, Dr. Lyons-Weiler. The prospect of these vaccines being widely distributed and used without even the minimal and wholly inadequate safety testing that other vaccines are subjected to is horrifying. Looks like the UK will be finishing off their elderly population forthwith, as guinea pigs for no other purpose than vast profits for pharma. There should be hard time in prison for the promoters of these vaccines. Perhaps the scaffold would be more appropriate.
Bravo Dr. Jack!
Thank you.
Thank you for making this information public!
Any insights on this study released on the NEJM blog:
Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine:
Original Article from The New England Journal of Medicine — Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine
Is this the raw data many have been asking for?
Thank you so much for your excellent work, James! I watched your explanation of your theories and methodologies regarding your study on long term health outcomes for vaccinated vs unvaccinated children. This, to me, is what genuine science is all about.
Over a period of years, I have been digging into all aspects of vaccines in general, including various historical records on specific diseases and vaccines. Since the ‘covid crisis’ emerged on the global stage, I’ve been digging into all aspects of this pandemic narrative, including the purported isolation, gene sequencing, and infectiousness in humans of the SA-CoV- 2 virus, and also the issues around the PCR tests and the mRNA vaccines. Obviously, all of these elements tie in with each other.
I have a number of observations and questions I would very much like to get your feedback on, but one thing stands our for me at the moment regarding these mRNA vaccines. Every single one of them stipulates that, in order to function as designed, they require a segment of the gene sequence SPECIFIC to the covid virus. However (and please correct me if I’m wrong), the gene sequence segment supposedly identified and being used is NOT specific to just this one corona virus strain.
If I am correct in this observation, then it could only amplify (by 40 cycles at least!) your point about pathogenic priming, since it would trigger this response not only to this one specific coronavirus, but an unknown number of coronaviruses (including any number that would be otherwise harmless in humans).
And that leads me to another key issue that I would like your feedback on, regardless of your take on whether or not the gene sequence being used for these mRNA vaccines is specific to the covid virus. This has to do with the alleged human infectiousness of the SA-CoV-2 virus. As far as I have been able to discover, there is only one study which is claimed to have demonstrated infectiousness in humans, this one here: https://wwwnc.cdc.gov/eid/article/26/6/20-0516_article?fbclid=IwAR1_KlNfYIA7LQJiMb3aYzgKSVJLX7FwuH6YQsKTBmYMr9ZV7S8IHvDlZlM
As I read it, what this study in fact has demonstrated is precisely the OPPOSITE, that the virus in question is NOT infectious in humans! In a nutshell, what they tell us is that the only cells that showed susceptibility to infection by their viral isolate were monkey kidney cells. The human cells showed NO CPE. The key words in that study are here: “No CPE was observed in any of the cell lines except in Vero cells”.
I’m not a biologist, and didn’t know the meaning of ‘CPE’, so I looked it up for myself and other laypersons: “Cytopathic effect or cytopathogenic effect (abbreviated CPE) refers to structural changes in host cells that are caused by viral invasion. The infecting virus causes lysis of the host cell or when the cell dies without lysis due to an inability to reproduce. Both of these effects occur due to CPEs.”
“Cell lysis is a common outcome of viral infection. It consists of a disruption of cellular membranes, leading to cell death and the release of cytoplasmic compounds in the extracellular space. Lysis is actively induced by many viruses, because cells seldom trigger lysis on their own.”
Here is the full quote from this study pertaining to their efforts to infect various cell lines, human and animal, with this virus:
“Because research has been initiated to study and respond to SARS-CoV-2, information about cell lines and types susceptible to infection is needed. Therefore, we examined the capacity of SARS-CoV-2 to infect and replicate in several common primate and human cell lines, including human adenocarcinoma cells (A549), human liver cells (HUH7.0), and human embryonic kidney cells (HEK-293T), in addition to Vero E6 and Vero CCL81 cells.
We also examined an available big brown bat kidney cell line (EFK3B) for SARS-CoV-2 replication capacity. Each cell line was inoculated at high multiplicity of infection and examined 24 h postinfection (Figure 3, panel A). No CPE was observed in any of the cell lines except in Vero cells, which grew to >107 PFU at 24 h postinfection. In contrast, HUH7.0 and 293T cells showed only modest viral replication, and A549 cells were incompatible with SARS-CoV-2 infection.
These results are consistent with previous susceptibility findings for SARS-CoV and suggest other common culture systems, including MDCK, HeLa, HEP-2, MRC-5 cells, and embryonated eggs, are unlikely to support SARS-CoV-2 replication (20–22). In addition, SARS-CoV-2 did not replicate in bat EFK3B cells, which are susceptible to MERS-CoV.”
Bear in mind that not only do they clearly state that the ONLY cell lines that show CPE lysing from that virus are those Vero (monkey kidney) cells, but they also state that “other common culture systems, including MDCK, HeLa, HEP-2, MRC-5 cells, and embryonated eggs, are unlikely to support SARS-CoV-2 replication”. Which explains why the CDC document states that “no quantified virus isolates of the 2019-nCoV are currently available” – they have no way to produce that isolated virus with the normal procedures used to create viral cultures. For the virus used in their study, they had to use, guess what? Monkey kidney Vero cells to produce their isolate, because “…these results suggest that VeroE6 cells might be the best choice for amplification and quantification, but both Vero cell types support amplification and replication of SARS-CoV-2.”
The process by which they claim to have fully sequenced the genome of this virus also appears to be highly dubious, but even if we accept as valid the premise that they have correctly sequenced the virus, and even if the gene sequence SEGMENT being used for these mRNA vaccines is indeed specific to this virus and not one shared by many other coronaviruses, it is nonetheless one which belongs to a virus which has been demonstrated to be non infectious in humans. I see no other rational conclusion to be derived from a close reading of the research, but I am always open to considering further information that might lead me to change my mind.
Stuart, studies have isolated the viral genome and sequenced it from many thousands of human samples now. The first of these studies, in China and the US, indepednently used shot-gun sequencing from samples from the lungs of people with a novel type of pneumonia – the radiography differed, the infection went deep into the alveoli to the periphery. There were glass-like opacities – not seen in other pneumonias (but, interestingly, see in measles). Importantly, they did NOT get other viral genomes out of these samples. See the report on my phylogenetic assessment in which I find a SARS-Cov-2 like spike protein in a “SARS” sequence from 2005 (report #2, here). Look around the blog here for other related articles explaining all of this. Note especially how the 2005 sequence was downloaded by Baric et al., in 2008, and that neither the scientists in Hong Kong nor in NC, USA knew they had something other than SARS. Baric used the HKU-3-3 sequence and three others to calculate a consensus sequence – ironically 3/4 – and generated a SARS rna molecule that could infect feline cell lines. They had to modify it a bit. I cannot address all of the other points, but here’s a study that I think will be of interest. https://pubmed.ncbi.nlm.nih.gov/32558946/
Thanks, James. Okay, I’ll take your word for it that the virus has been sequenced. Can you tell me if the gene sequence fragment being used in these mRNA vaccines is specific to this particular virus, and is definitely not a fragment that is shared with other coronaviruses? This is an important question, right? Correct me if I’m wrong, but if it is shared by other coronaviruses, the vaccines would trigger pathogenic priming for those as well, right?
And what about the purported infectiousness of the virus? Do you know of any other studies besides the one I quoted which in effect claims to demonstrate the (partial) fulfillment of Koch’s postulate by demonstrating the infectiousness of SA-Cov 2 in humans?
After reading the study I cited and my analysis of it, what is your take on that?
Do you have any input/insight into the question of molecular mimicry and fertility? (Similarities between syncyctin and the spike protein being a concern?)
yes please comment about the syncytin homology.
Excellent Work. Thank you.. beyond words…for all your articles.
How is it possible that these crimes are not being stopped? Millions will die.