Pathogenic Priming Verified, Again
Study on unvaccinated people who had mild COVID-19 show that all of them had auto-antibodies
Pathogenic priming, as I predicted in April, 2020, has been verified, again.
Many people ask me: “How did you publish a peer-reviewed study on the SARS-CoV-2 virus merely three months after the world learned about the virus”? It’s actually an interesting story.
At the end of January, 2020, I was in the Seattle airport returning from a speaking tour. We were about twenty minutes away from boarding, and I left the gate to pick up a coffee. On that way back, I ran into a group of six or seven Chinese men, all about six feet tall. All were masked. Ominously, one was crumpled on the ground, against the wall, sobbing.
Before the plane left the tarmac, I had searched online and found the news about a new virus that was causing problems in Wuhan, China.
About a week later, I fell ill. If you go back to my podcasts at the time, I had a persistent, dry cough. Nothing would ease the cough. I was sick for a long, long time. We did not yet know that loss of sense of taste and smell was a symptom of COVID; the virus was still being called “Wuhan nCoV-19 virus”. Finally, one evening, I told Gracie that I felt that I was drowning. I was a bit delirious. That night, I spiked a very high fever - and the next day, I began to feel better. I had a long recovery - a few months - and, naturally, I thought perhaps I had had this new virus.
While I was sick, I told my sons to not come to the house. I slept separate from Gracie, we sanitized surfaces. She did not get sick.
Now, I don’t know 100% that I had COVID-19. I think perhaps I did. If so, mine could have been one of the first cases in the US.
When the genomic sequence of the new virus was published, I realized I had an opportunity to ask the question: how does it cause its unusual disease features? Unlike most respiratory viruses, this one damaged lung tissue to the periphery of the alveoli, the little balloon where gas exchange takes place. It seemed to also have disease features such as a prolonged prodromal period - the period of time between exposure and first symptoms. It seemed to be particularly dangerous to the elderly and to people with diabetes (recall the reported 20% risk of death in people with diabetes?).
My research opportunity was in the area of autoimmunity. I realized that if I could identify the parts of the viral proteins that were capable of eliciting a B-cell response, I could then check those viral epitopes for matches to human proteins. The sequence was published in March 2020; as soon as it was published, I did my analysis and wrote it up, and sent it to a journal for peer-review. The journal’s reviewers saw it fit for publication, but one insisted that I report that Pathogenic Priming from vaccination was only a theoretical possibility (no vaccine had been given EUA by that time). I had reported that exposure via either infection or injection could risk autoimmunity. I had pointed out precisely how - and reported the parts of the proteins that should not be included in any vaccine.
A study by Vojdani et al. (Harvard University) validated my specific predictions: yes, the virus contain proteins, including the spike, that will likely cause autoimmunity in humans.
Now, another study has found that exposure to SARS-CoV-2 proteins can lead to autoimmunity. Researchers at Cedars Sinai have reported a study that further validates that autoimmunity is a risk in virtually all cases of mild COVID. In their study of people who had asymptomatic, mild and more-than-mild COVID-19 in the pre-vaccine era, the researchers found autoimmune antibodies. The study is missing a few key details, such as which autoantibodies map to individual viral proteins, however, past studies showed that the spike protein is second only to the nucleocapsid protein in terms of a source of the number of identifiable autoreactive epitopes (what I call “unsafe epitopes").
I may write to the authors for their data, which they promise is available to anyone interested, to see if I can determine the distribution of how the autoantibodies detected target unsafe epitopes.
However, the study fails to mention that vaccines contain SARS-CoV-2 proteins. Some of the vaccines contain the entire proteomic repertoire; the mRNA vaccines encode just the spike, but the spike itself has more unsafe epitopes than any other SARS-CoV-2 protein except the nucleocapsid protein.
The concept of Pathogenic Priming should lead one to reduce, as much as possible, the risk of re-exposure to the same proteins that might prime the autoimmunity.
Thus, the policies that lead to vaccination of those who are already immune (survivors of COVID-19) should be changed, with haste, especially given that natural immunity confers long-lasting protection. And it must be considered by those adopting enforceable public health policies that mass vaccination causes all of the priming by vaccination to occur in a compressed time period.
To my knowledge, none of the vaccine manufacturers have bothered to remove the autoreactogenic epitopes. This includes the Novavax vaccine, which is an injection of microparticles that contain the actual spike protein and a relatively new vaccine adjuvant, M-matrix, which is based on saponin extracted from the soapbox tree (Quillaja saponaria). It turns out that some people who are allergic to quinoa have a saponin allergy - thus, it would be important for physicians considering offering the Novavax vaccine, and patients considering taking it, to be aware of whether they are in fact allergic to saponin. It’s possible and perhaps even likely that some who accept this new vaccine will develop allergic responses to saponins and may develop new food allergies. No data on that yet, but it is entirely reasonable to expect that outcome.
My take-home messages is that people may want to mute their inevitable SARS-CoV-2 virus infection with early aggressive treatments to reduce the severity of the illness, but also to reduce the likelihood of the development of autoimmunity from pathogenic priming, and that mass intentional exposure of entire populations to viral proteins with a vaccine should be expected to lead to increased risk chronic morbidity when the virus finds the vaccinated.
References
Study: Paradoxical sex-specific patterns of autoantibody response to SARS-CoV-2 infection https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-03184-8
Lyons-Weiler J. Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity. J Transl Autoimmun. 2020 Apr 9;3:100051. doi: 10.1016/j.jtauto.2020.100051. PMID: 32292901; PMCID: PMC7142689.
Vojdani, A, E Vojdani and D Kharrazian. 2021. Reaction of Human Monoclonal Antibodies to SARS-CoV-2 Proteins With Tissue Antigens: Implications for Autoimmune Diseases Frontiers in Immunology https://doi.org/10.3389/fimmu.2020.617089
Cedar Sinai Press release:
https://www.cedars-sinai.org/newsroom/covid-19-can-trigger-self-attacking-antibodies/
I developed autoimmunity after natural infection.
In 1985, after experiencing a particularly severe strep throat infection,approximately three weeks later,I developed Guttate Psoriasis, which the Dermatologist referred to as "a post-streptococcal rash" The rash was extensive, covering around 90% of my body and lasted approximately 3 months, being treated with topical cortisone for the entire time.
Fast forward to January 2018, and again I developed Guttate Psoriasis three weeks after experiencing a relatively mild common cold. This time I did not suppress the rash with cortisone, and instead exposed my skin to sunlight. The rash resolved in about 10 and 1/2 months.
Fast forward again to January 2022, and I again developed a common cold. No rash yet, and hopefully the protocols I used to treat the cold this time, will prevent the provocation of my immune system into autoimmunity.
Pathogenic Priming is a general category; it is sensitization of people (or animals) to illness of any kind due to an exposure to pathogenic proteins (or parts of proteins), which then manifests upon a second exposure to the same or similar protein or protein part at a later time. ADE is a specific type of PP that involves antibodies making an infection worse by making cell entry easier. PP can involve autoimmunity; ADE does not.