There is growing evidence that self-attacking ‘autoantibodies’ could be the key to understanding some of the worst cases of COVID-19.
This might explain why lung damage and other organ damage sometimes continues to worsen AFTER the body seems to have cleared the SARS-CoV-2 virus. And it could explain why some individuals fail to mount an adequate immune response early in the disease.
With respect to the later, in September 2020 researchers at the Rockefeller University reported that > 10% of 987 patients with severe COVID-19 infection had antibodies that blocked type 1 interferon molecules, an essential part of the innate immune system.
Other researchers have screened patients with varying severity of COVID-19 and found higher prevalence of autoantibodies against the immune system in infected individuals compared to uninfected controls.
Yet another study found that some infected individuals had autoantibodies against proteins in their blood vessels, heart and brain.
Many patients with severe COVID suffer from life threatening blood clots. Phospholipids play a major role in controlling blood clotting. 52% of 172 people hospitalzied with COVID 19 were found to have anti-phospholipid antibodies.
Annexin A2 is a human protein that protects the integrity of small blood vessels in the lung. Researchers have found a significantly higher average level of anti-annexin A2 antibodies in people who died of COVID-19 compared to patients with less severe illness.
So far it is unclear whether the virus caused these antibodies or whether these unlucky individuals had higher than normal amounts of auto-antibodies prior to infection.
A paper published in the immunology literature just yesterday might shed some light on this issue as well as on the topic of LONG COVID.
We sought to determine whether immune reactivity occurs between anti-SARS-CoV-2 protein antibodies and human tissue antigens, and whether molecular mimicry between COVID-19 viral proteins and human tissues could be the cause.
In other words, they tested antibodies against the SARS-CoV-2 virus to see whether they reacted against various kinds of human tissue. Here is what they found.
We found that SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues, and more.
This extensive immune cross-reactivity between SARS-CoV-2 antibodies and different antigen groups may play a role in the multi-system disease process of COVID-19, influence the severity of the disease, precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases.
You can read the full study here: https://www.frontiersin.org/articles/10.3389/fimmu.2020.617089/full
Cross reactivity between antibodies against COVID-19 virus and human tissue was found for every major organ system in the human body.
The concept of “molecular mimicry” has been well described in auto-immunity for many years. This occurs when a portion of a foreign protein (on for example a virus or bacterium) is identical to a portion of a protein found in human tissue. When the immune system responds to invasion by a virus or bacteria it creates antibodies to various proteins on the invader. But in so doing the anti-bodies can react against human tissue that shares a small common string of amino acids (referred to as an epitope).
A famous example of molecular mimicry occurs with Rheumatic Heart Disease in which antibodies against the bacteria responsible for Strep Throat cross react with heart tissue causing destruction of heart valve tissue and a resultant leaky heart valve. In this situation cross reaction can also occur with tissue in joints resulting in arthritis, another hallmark of rheumatic fever. These were serious complications of Strep Throat before Penicillin became widely available.
So far we know that sicker COVID-19 patients demonstrate antibodies against multiple types of human tissue.
We also know that antibodies that react against various portions of the virus can also react against human tissue.
Finally we know that multi-organ failure is an inflammatory response wherein the immune system, rather than the virus, causes organ failure.
It would be a reasonable conclusion that auto-immunity can acutely contribute to cytokine and bradykinin storm.
It would also be a reasonable conclusion that auto-immunity contributes to LONG COVID.
So why would that make an mRNA vaccine safer?
The mRNA vaccine results in antibodies against one part of the virus (one epitope, the spike protein).
But infection results in antibodies against MULTIPLE PARTS OF THE VIRUS (multiple epitopes). Because multiple antigens or epitopes are involved in the immune response to infection, it increases the probability that cross reaction with multiple human tissues can result.
From an autoimmune perspective, the mRNA vaccine is much safer.
Obviously, given the fact that over 400,000 deaths have resulted in the US from this infection and no deaths have been attributed to the vaccine, the vaccine appears to be much safer than infection. Both the Pfizer and Moderna vaccine have decreased the risk of symptomatic infection by 95%. Severe symptomatic infection can lead to death. Even asymptomatic infection can cause LONG COVID. The risk-benefit analysis overwhelmingly favors the vaccine.
For a deeper dive into auto-immunity and COVID-19 here are a few more references:
High frequency of cerebrospinal fluid autoantibodies in COVID-19 patients with neurological symptoms
Autoantibodies against type I IFNs in patients with life-threatening COVID-
Diverse functional autoantibodies in patients with COVID-19
Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19
Association between anti-interferon-alpha autoantibodies and COVID-19 in systemic lupus erythematosus
Autoantibodies related to systemic autoimmune rheumatic diseases in severely ill patients with COVID-19
IgM autoantibodies recognizing ACE2 are associated with severe COVID-19
Is the association between IgG anti‐cardiolipin autoantibodies and COVID‐19 severity related to the lung injury or to the SARS‐CoV‐2 infection?
Do cross-reactive antibodies cause neuropathology in COVID-19?
Immunoserologic detection and diagnostic relevance of cross-reactive autoantibodies in coronavirus disease 2019 patients
Anticardiolipin IgG Autoantibody Level Is an Independent Risk Factor for COVID‐19 Severity
Rheumatic manifestations of COVID-19: a systematic review and meta-analysis
The immunology of multisystem inflammatory syndrome in children with COVID-19
Clinical, Serological, and Histopathological Similarities Between Severe COVID-19 and Acute Exacerbation of Connective Tissue Disease-Associated
In the context of the COVID 19 pandemic I will close with the usual summary.
- Avoid alcohol consumption (alcohol wreaks havoc with your immunity)
- Get plenty of sleep (without adequate sleep your immune system does not work well )
- Follow good sleep habits
- Exercise, especially out of doors in a green space, supports the immune system
- Get some sunshine and make sure you have adequate Vitamin D levels. Supplement with Vitamin D3 to get your levels above 30 ng/ml. (read this Open Letter)
- Eat an anti-inflammatory diet rich in micronutrients.
- Practice stress reduction like meditation and yoga which improves the immune system
- Eliminate sugar-added foods and beverages from your diet. These increase inflammation, cause metabolic dysfunction, and suppress immunity.
- Eliminate refined-inflammatory “vegetable oils” from your diet, instead eat healthy fat.
- Clean up your home environment and minimize your family’s exposure to environmental toxins by following recommendations at EWG.org with regards to household products, personal care products, and organic foods. (https://www.ewg.org/)
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Eat clean, drink filtered water, love, laugh, exercise outdoors in a greenspace, get some morning sunlight, block the blue light before bed, engage in meaningful work, find a sense of purpose, spend time with those you love, AND sleep well tonight.