A newly released study, Autoantibodies linked to autoimmune diseases associate with COVID-19 outcomes, discovered elevated autoantibodies in patients with moderate to severe COVID-19 infections.[1]
The study included 248 adults from five states of the USA. One hundred seventy-one of them had COVID-19 symptoms and tested positive for SARS-CoV-2 by PCR testing. Seventy-seven are healthy controls.
The subjects were classified according to the World Health Organization (WHO) COVID-19 disease severity classification as:
- Mild COVID-19 (n=74; fever duration ≤ 1 day; peak temperature of 37.8 C)
- Moderate COVID-19 (n=63; fever duration ≥ 7 days; peak fever of ≥ 38.8 C)
- Severe COVID-19 groups (n=32; severe symptoms and requiring supplemental oxygen therapy)
Blood from the study subjects was collected before they had their COVID-19 shots. Their serum was tested for IgG and IgA antibodies to the SARS-CoV-2 spike and nucleoproteins. The same antibodies were also tested against several human body proteins to see if they would cross-react. If cross-reaction happens, the autoantibodies can potentially attack the organs that contain those proteins and cause autoimmune disease.
Statistical analyses were done for correlation between antibodies and disease severity.
Results
Higher autoantibodies in certain groups
The study found that there are people who develop more autoantibodies, and they are:
- Those who had moderate to severe COVID-19 had more autoantibodies.
- People who lost their sense of smell (anosmia) also had more autoantibodies.
- Older people (≥60) who recovered from moderate to severe CV19 have more autoantibodies than the younger group (<60).
- People with more significant numbers of IgG and IgA antibodies.
Autoantibodies after COVID-19 and resulting Autoimmune diseases
The following are the autoantibodies detected and the autoimmune diseases that can potentially result from them.
- Alzheimer’s disease – (rabaptin-5, tau protein)
- Antiphospholipid syndrome – (cardiolipin)
- Celiac disease – (transglutaminases, zonulin)
- Gut motility disorders – (enteric nerve)
- Immune thrombocytopenia – (platelet glycoprotein)
- Immune thrombotic thrombocytopenia – (heparin)
- Liver autoimmunity – (liver microsomal antigen)
- Multiple sclerosis and other neuroimmune disorders – (myelin basic protein)
- Myasthenia gravis – (acetylcholine receptor, somatotropin)
- Neurodegenerative diseases – (neurofilament proteins)
- Neurological disorders – (S100B)
- Neuropsychiatric and neurodegenerative disorders – (NMDAR)
- Parkinson’s disease – (α-synuclein)
- Pemphigus vulgaris or foliaceus – (Desmoglein-E-Cadherin 1)
- Rheumatic heart disease – (α-myosin)
- Rheumatoid arthritis – (α-enolase, fibulin)
- Systemic lupus erythematosus – (cardiolipin, dsDNA, rabaptin-5)
- Type 1 diabetes – (islet cell antigen)
- Vitiligo – (tyrosinase)
Many of these diseases are in The Complete List of the Pfizer Adverse Events of Special Interest that should be reported to VAERS to determine if the CV19 shots are safe or else they will be included in the yearly vaccination schedule.
Not all autoantibodies in the study were elevated. Autoantibodies like α-myosin, rabaptin-5, S100B, cerebellar, and IgA autoantibodies targeting the NMDA receptor and cerebellar were reduced in other subjects. To the authors, this indicates “a broad breakdown of physiological autoantibody levels/self-tolerance in patients with COVID-19 that paralleled disease severity.”
Autoimmune diseases after COVID-19
The study’s findings explain why some people who recovered from COVID-19 later develop autoimmune diseases, as shown in the list below. Case reports of people developing autoimmune diseases have been published. The links to the case reports are embedded in each condition.
- Antiphospholipid syndrome
- Autoimmune hemolytic anemia
- Gullain-Barré syndrome
- Graves’ disease
- Immune thrombocytopenic purpura
- New-onset type 1 diabetes
- Polyneuritis cranialis
- Systemic lupus erythematosus
- Viral Arthritis
These findings are consistent with the notion that autoantibodies are natural
components of human physiology and become dysregulated under disease conditions.[1]
Why did autoimmune antibodies go up?
The authors offered three mechanisms: molecular mimicry, epitope spreading, and bystander activation. Molecular mimicry is when the protein sequences in the virus are similar to human proteins.
Epitopes are sites on the substance that elicit an immune response. Epitope spreading refers to developing an immune response to epitopes distinct from, and non-cross-reactive with, the disease-causing epitope. [3] That is in contrast to molecular mimicry, where the antibodies directed against a virus can also attack the host.
Bystander activation is when the T cells and B cells become involved in an antigen-independent manner. This happens based on an individual’s genetic interaction with his environment over time.
If antibodies developed during COVID-19 can cause autoimmune disease, can it also happen after COVID-19 “vaccinations”?
The featured study [1] did not mention autoimmunity resulting from the CV19 injections.
In another research, Immune-Mediated Disease Flares or New-Onset Disease in 27 Subjects Following mRNA/DNA SARS-CoV-2 Vaccination [4] reports 27 cases included 17 flares and ten new-onset immune-mediated diseases.
23/27 received the Pfizer BNT-162b2 vaccine, 2/27 the Moderna mRNA-1273, and 2/27 the Astra Zeneca ChAdOx1 vaccine. 80% resolved with corticosteroid therapy. [4]
There were four cases of Behcet’s disease, 3 cases of systemic lupus erythematosus, and dermatomyositis. There were three new-onset vasculitis cases, including a Henoch-Schönlein Purpura and two instances of chilblain lesions. [4]
One new case of polymyalgia rheumatica (PMR) was reported, and 1 case of remitting seronegative symmetrical synovitis with pitting edema (RS3PE) (new-onset) was documented in a subject with confirmed PMR that was treated 15 years earlier. [4]
Other immune-mediated conditions included idiopathic pericarditis (n = 2), neurosarcoidosis with small fiber neuropathy (n = 1), demyelination (n = 1), and myasthenia gravis (n = 2)[4]
Other non-rheumatologic diseases are myasthenia gravis, multiple sclerosis, neurosarcoidosis and small fiber neuropathy, and pericarditis. [4]
In another study, 1,377 patients with rheumatic and musculoskeletal diseases (RMDs) were surveyed, and 11% reported a flare-up of their disease following 2-dose SARS-CoV-2 messenger RNA (mRNA) vaccination. Flares were associated with prior SARS-CoV-2 infection. This makes sense since the CV19 shots elicited more significant amounts of antibodies that explain the exacerbations. [5]
Mechanisms of COVID-19 vaccines autoimmunity
A review paper explained that the adjuvants used in the vaccines are toll-like receptor agonists (TLR7/8) involved in the generation and amplification of autoreactive immune responses.[5]
TLR7 and TLR9 can also elevate the levels of type I interferon and upregulate interferon‐stimulated genes that participate in the mechanisms of several rheumatic diseases. [5]
Something to think about
The study by Baiocchi and colleagues [1] found that higher levels of autoantibodies and risk of autoimmune diseases correlate with greater amounts of antibodies. COVID-19 booster shots do exactly the same thing.
People who had autoimmune conditions after their previous shots should have a heart-to-heart talk with their physicians about whether the benefits will outweigh the risk of a flare-up.
Parting thoughts
At the beginning of the roll-out of the COVID-19 injections, I did my research to see if the shots are safe or not. My investigation resulted in the following articles that I posted in January 2021.
- COVID-19, Autoimmunity and Vaccination, Part 1
- COVID-19, Autoimmunity, and Vaccination Part 2
- COVID-19, Autoimmunity, and Vaccination Part 3
- Molecular Mimicry between the SARS-CoV-2 and the Breathing Center
- Molecular mimicry between the spike protein and humans can shut down platelet production
I wrote them to inform and warn my readers. At that time, the autoimmune risks were theoretical. Now they are real.
Truth heals. Lies kill. Don’t Get Sick!
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- Guillain-Barre Syndrome After Covid-19 Vaccination
- Study: SARS-CoV-2 Spike Proteins Impaired DNA Repair That Can Lead to Defective Immunity and Cancers
- Comparison of Adverse Reactions of Seven Types of COVID-19 Vaccines in the Philippines
- The High Risk of Deadly Brain Clots in the J & J COVID Vaccine
- Lot Numbers of Pfizer and Moderna mRNA Vaccines with the Highest Deaths
- Adverse Reactions to Pfizer Biontech Vaccine for the 5-11 Years Old
- Kounis syndrome can explain vaccine-related heart attacks
- Myocarditis after mRNA Vaccination in the Military
References:
- Baiocchi et al. Autoantibodies linked to autoimmune diseases associate with COVID-19 outcomes.
- Sachinidis A, Garyfallos A. COVID-19 vaccination can occasionally trigger autoimmune phenomena, probably via inducing age-associated B cells. Int J Rheum Dis. 2022;25(1):83-85. doi:10.1111/1756-185X.14238
- Powell AM, Black MM. Epitope spreading: protection from pathogens, but propagation of autoimmunity? Clin Exp Dermatol. 2001 Jul;26(5):427-33. doi: 10.1046/j.1365-2230.2001.00852.x. PMID: 11488833.
- Watad et al. Immune-Mediated Disease Flares or New-Onset Disease in 27 Subjects Following mRNA/DNA SARS-CoV-2 Vaccination. Vaccines (Basel). 2021 Apr 29;9(5):435. doi: 10.3390/vaccines9050435. PMID: 33946748; PMCID: PMC8146571.
- Connolly CM et al. Disease Flare and Reactogenicity in Patients With Rheumatic and Musculoskeletal Diseases Following Two-Dose SARS-CoV-2 Messenger RNA Vaccination. Arthritis Rheumatol. 2022 Jan;74(1):28-32. doi: 10.1002/art.41924. Epub 2021 Dec 3. PMID: 34346185; PMCID: PMC8712346.