As your immune system fights off an infection (or an injection…) it can make a mistake and decide to attack some of your cells / parts as well. This effect is increased the more the invader has proteins similar to yours. There’s a load of different auto-immune diseases that this might cause or increase. This is called Pathogenic Priming.
It looks like Chinese Wuhan Covid-19 is a good candidate for pathogenic priming. As is the vaccine for it. It may well take a year or so to find out the degree. FWIW, an Epitope is the part of an antigen (usually a chunk of protein) that your immune system latches on to.
An epitope, also known as antigenic determinant, is the part of an antigen that is recognized by the immune system, specifically by antibodies, B cells, or T cells. For example, the epitope is the specific piece of the antigen to which an antibody binds. The part of an antibody that binds to the epitope is called a paratope. Although epitopes are usually non-self proteins, sequences derived from the host that can be recognized (as in the case of autoimmune diseases) are also epitopes.
Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity
• All SARS-CoV-2 immunogenic epitopes have similarity to human proteins except one.
• Roughly one-third of the potentially targeted human proteins (putative autoantigens) are key players in the adaptive immune system.
• The list of viral/human protein matches provides clues on which epitopes or parts of epitopes might be involved in the immunopathogenesis of COVID-19 disease from SARS-CoV-2 infection.
• It also indicates which epitopes might be responsible for autoimmunological pathogenic priming due to prior infection or following exposure to SARS-CoV-2 or relatives following vaccination.
• These epitopes should be excluded from vaccines under development to minimize autoimmunity due to risk of pathogenic priming.
So “all but one” ought to be excluded from vaccines to “minimize autoimmunity due to risk of pathogenic priming” eh? And are they?
Homology between human and viral proteins is an established factor in viral- or vaccine-induced autoimmunity. Failure of SARS and MERS vaccines in animal trials involved pathogenesis consistent with an immunological priming that could involve autoimmunity in lung tissues due to previous exposure to the SARS and MERS spike protein. Exposure pathogenesis to SARS-CoV-2 in COVID-19 likely will lead to similar outcomes. Immunogenic peptides in viruses or bacteria that match human proteins are good candidates for pathogenic priming peptides (similar to the more diffuse idea of “immune enhancement”). Here I provide an assessment of potential for human pathogenesis via autoimmunity via exposure, via infection or injection. SAR-CoV-2 spike proteins, and all other SARS-CoV-2 proteins, immunogenic epitopes in each SARS-CoV-2 protein were compared to human proteins in search of high local homologous matching. Only one immunogenic epitope in a SARS-CoV-2 had no homology to human proteins. If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development. Mapping of the genes encoding human protein matches to pathways point to targets that could explain the observed presentation of symptoms in COVID-19 disease. It also strongly points to a large number of opportunities for expected disturbances in the immune system itself, targeting elements of MHC Class I and Class II antigen presentation, PD-1 signaling, cross-presentation of soluble exogenous antigens and the ER-Phagosome pathway. Translational consequences of these findings are explored.
The pdf can be downloaded free at the link.
Bottom line is that this virus targets the immune system to some degree and vaccines that attack those proteins are very likely to cause an autoimmune problem too.
Innate immunity is far more important in defeating this virus, and focusing on antibody creation to the viral proteins may well be sub-optimal in several ways.
But how common is this autoimmunity thing? Are we talking Zebras or Horses?
Prevalence of autoantibody responses in acute coronavirus disease 2019 (COVID-19)
Angelica Lerma, Anu Chaudhary, Andrew Bryan, Chihiro Morishima, Mark H.Wener, Susan L.Fink
• Autoantibodies against nuclear antigens are detectable in 25% of patients hospitalized with acute COVID-19.
• Anti-nuclear antigen antibodies were weakly reactive and most often directed to single antigens.
• Vasculitis-associated autoantibodies were not detected in specimens from patients with acute COVID-19.
• Anti-phospholipid antibodies were infrequently detected in patients with acute COVID-19.
OK, so if you are bad enough off to end up in the hospital, it is about 25%. So you really want to avoid being that bad. This implies tuning up your innate immune system (Vit-D, Vit-C, Vit-E, Zinc, Selenium, etc.) and treating any symptoms very early with the application of zinc ionophores and antivirals (HCQ, Quercitin, Quinine, Ivermectin, Doxycycline, Azithromycin, etc. for example in some combination as directed by your M.D. of choice.)
Could this also explain the tendency for some folks to “go down” in a strong immunity reaction to the vaccine? Not just an anaphylactic shock reaction to the viral protein, but a tendency to start seeing a lot of ‘self’ as invader proteins? Or that Florida M.D. who died a couple of weeks after his vaccination via zero blood platelets in acute thrombocytopenia?
What percentage of those vaccinated who die, or end up with lupus, arthritis, M.S., damaged immune systems, etc. is acceptable? Where are the numbers?
IF, as looks the case, under 10% of folks infected actually manifest disease and of them another 10% go to hospital and even fewer die, are we not looking at a fraction of a percent? So is the autoimmune “side effect” of a vaccine higher or lower than that?
Immunopathology may play a significant role in the pathogenesis of Coronavirus-Induced Disease-19 (COVID-19). Immune-mediated tissue damage could result from development of rapid autoimmune responses, characterized by production of self-reactive autoantibodies. In this study, we tested specimens from acutely ill patients hospitalized with COVID-19 for autoantibodies against nuclear, vasculitis-associated, and phospholipid antigens. Detectable autoantibodies were present in 30% of the patients in our cohort, with the majority of reactive specimens demonstrating antibodies to nuclear antigens. However, antinuclear antibodies were only weakly reactive and directed to single antigens, as is often seen during acute infection. We identified strongly reactive antibodies to nuclear antigens only in patients with a prior history of autoimmune disease. In our cohort, the prevalence of antiphospholipid antibodies was low, and we did not detect any vasculitis-associated autoantibodies. We found similar levels of inflammatory markers and total immunoglobulin levels in autoantibody positive versus negative patients, but anti-SARS-CoV-2 antibody levels were increased in autoantibody positive patients. Together, our results suggest that acute COVID-19 is not associated with a high prevalence of clinically significant autoantibody responses of the type usually associated with autoimmune rheumatic disease.
What about a type not “usually associated with autoimmune rheumatic disease” but perhaps with other modes such as destruction of white blood cells? Eh?
So if you already have an autoimmune issue, it is worse, but for most folks it looks like the level of autoimmune response is not “clinically significant”. Well that’s good to know. BUT, what is the extent of ‘outlier’ cases? As a person with mild autoimmunity issues (arthritis) and a VERY active immune system, am I likely to be the 1 in 1000 that pops the cork? Eh? I’d like to know that before I get an injection of autoimmunity stimulating virus stuff…
There does seem to be a precedent for vaccinations causing “issues”:
Gulf war illness, post-HPV vaccination syndrome, and Macrophagic Myofasciitis. Similar disabling conditions possibly linked to vaccine-induced autoimmune dysautonomia.
Manuel Martinez-Lavin, Melina Tejada-Ruiz
• All original investigations reported a link between vaccines and Gulf War Illness.
• Post-HPV Vaccination Syndrome and Macrophagic Myofasciitis resemble Gulf War Illness.
• Chronic fatigue, widespread pain and dyscognition characterize these three illnesses.
• Small fiber neuropathy and anti-adrenergic receptor antibodies are linked to Post-HPV Vaccination syndrome.
• Hypothesis: Vaccine-induced autoimmune dysautonomia may be the common underlying mechanism.
More than one-fourth of all Persian gulf war coalition soldiers remain seriously ill. Several epidemiological studies suggest a link between multiple vaccinations at the time of the military operation and the illness development. Macrophagic Myofasciitis and post-HPV vaccination syndrome are two newer controversial vaccine-related disabling ailments.
1) To systematically review all original articles investigating the association of vaccines with gulf war illness, 2) To discuss gulf war illness, Macrophagic Myofasciitis, and post-HPV vaccination syndrome clinical similarities, 3) To discuss emergent pathogenetic mechanisms proposed for post-HPV vaccination syndrome that may be also relevant to gulf war illness and Macrophagic Myofasciitis.
Results: All original epidemiological studies (n = 11) found a positive association between vaccination and gulf war illness development. Chronic fatigue, widespread pain and cognitive impairment characterize the three syndromes under discussion. Anti-adrenergic receptor antibodies, dysautonomia and small fiber neuropathy have been recently described in patients with post-HPV vaccination syndrome.
post-HPV vaccination syndrome, Macrophagic Myofasciitis, and gulf war illness analogy suggests that some vaccines or multiple vaccinations in a very short period of time may induce, in susceptible individuals, chronic pain, fatigue and dyscognition. Vaccine-induced autoimmune dysautonomia is hypothesized as the common pathogenetic mechanism for this symptom cluster. Further research on the presence of small fiber neuropathy, adrenergic receptor antibodies, and abnormal autonomic function tests in the three syndromes under discussion may help to elucidate this hypothesis.
Not quite a “smoking gun” but you can smell the burnt powder from here. Then there’s that small matter of injecting aluminum into your blood bypassing your gut barrier…
Imaging of aluminium and amyloid β in neurodegenerative disease
Christopher Exley, Matthew J.Mold
Recent research has confirmed the presence of aluminium in human brain tissue. Quantitative analyses suggest increased brain aluminium content in a number of neurodegenerative diseases including familial Alzheimer’s disease, congophilic amyloid angiopathy, epilepsy and autism. Complementary aluminium-specific fluorescence microscopy identifies the location of aluminium in human brain tissue and demonstrates significant differences in distribution between diseases. Herein we combine these approaches in investigating associations between aluminium in human brain tissue and specific disease-associated neuropathologies.
We have used aluminium-specific fluorescence microscopy, Congo red staining using light and polarised light and thioflavin S fluorescence microscopy on serial sections of brain tissues to identify co-localisation of aluminium and amyloid β and tau neuropathology.
A combination of light, polarised and fluorescence microscopy demonstrates an intimate relationship between aluminium and amyloid β in familial Alzheimer’s disease but not in other conditions and diseases, such as congophilic amyloid angiopathy and autism. We demonstrate preliminary evidence of amyloid β pathology, including associations with vasculature and parenchymal tissues, in autism in tissues heavily loaded with aluminium.
We suggest that complementary aluminium-specific fluorescence microscopy may reveal important information about the putative toxicity of aluminium in neurodegenerative and neurodevelopmental disorders.
So is it really a good idea to be repeatedly injecting a load of Aluminum into folks with every vaccination and then requiring they get dozens of them?
We evolved in a world FULL of aluminum. Aluminium is one of the most common elements in most rocks of the world. BUT, it doesn’t like to come out of the rocks and it doesn’t like to cross the gut into our blood. We remove the aluminum from the rocks, then put it into vaccines (as our bodies react to it quite strongly as a Bad Thing) and run around injecting it into everyone.
Somehow this doesn’t sound like a good idea to me.
Especially given that it is now associated with messed up proteins (Amyloid plaque) in messed up brains.
I am NOT an “Anti-Vaxer”. I’ve had all my shots, as have my kids. I’m very appreciative of the fact that they prevented me from experiencing small pox (yes, I’m old enough to have that vaccination) and a few other diseases; and that they prevented my kids from experiencing the Measles, Mumps and more that I had as a kid.
Vaccines are GOOD.
But we do need to recognize that not ALL vaccines are good and not ALL methods of making them are the best and that SOME folks get killed or damaged by vaccination, so it is not an unvarnished good.
A good friend spent most of her life in a wheel chair as a reaction to the early polio vaccine, for example. In some ways, her life for mine. That kind-of sucks.
What I’m asking for is a sober, considered, and objective risk / reward evaluation. Think about what we are doing and ask is it REALLY the best way and is it REALLY a good cost / benefit ratio? And is there a way to remove some or all of the risks?
Like, for example, asking just how much less effective is a vaccine without aluminum in it, and is that better than the ever increasing levels of Alzheimer’s and Autism? Ought we, perhaps, run an experimental group of folks who do not get aluminum in their vaccinations and get the answers, instead of just assuming we know?
FWIW, I do not plan to get the EXPERIMENTAL Chinese Wuhan Covid-19 vaccination. Why? I have a very active immune system. I have a small tendency to autoimmunity. I also tend to ‘throw off’ viruses quite quickly and easily. Plus I’ve got a supply of the necessary materials to defeat the virus with innate immunity and not proceed to antibody mediated immunity (and potential autoimmunity).
Essentially I’m more willing to be a “guinea pig” for the innate immunity boosters path than for the experimental potentially autoimmunity inducing vaccine path. My body, my choice. (To borrow a phrase from The Left…)