COVID-19 Autoimmunity: The Big Picture

February 18, 2021

From Ahvie Herskowitz, MD

There are long lists of microbes that cause autoimmune responses in humans- some examples are Lyme, Rubella, HIV, EBV, CMV, HSV-6, Hep A and C, Parvoviruses, Enteroviruses, Coxsackievirus, and Mycoplasma.

COVID-19 is now perhaps the most important of these since we already have 28 million infections in the USA, and even a small subpopulation of roughly 5% of infections occurring in persons being susceptible- that estimates to more than 1 million possible occurrences of autoimmunity.

COVID-19 induced autoantibody production can take place months after the acute infection is resolved. Autoantibodies are immune proteins produced by an individual’s immune system that target and attack the individual’s own tissues. These autoantibodies are normally associated with autoimmune conditions, such as rheumatoid arthritis and lupus, but in the case of a virus, such as COVID-19, the virus both activates the inflammatory pathways of the immune system and suppresses the normal regulation of inflammation- this is called “immune dysregulation.” These factors result in a cascade of autoantibody production that in turn may develop into long-term autoimmune conditions that attack the body.

There are two factors to COVID-19 and autoimmunity:

Direct COVID-19 Infection and Autoimmunity (Short-Term)

Direct, viral induced inflammation, after the virus can no longer be identified, leads to lung, heart, brain (neuro-inflammation and cognitive decline), gastrointestinal and liver conditions, and inflammation of blood vessels (endotheliitis). A recent study showed microvascular injury in the brains of patients with COVID-19, and another study showed myocarditis, or inflammation of the heart muscle, in COVID-19 patients as well. This is to be anticipated with any virus that produces organ injury, even when the virus cannot be cultured.

Indirect COVID-19 Infection and Autoimmunity (Post-Viral, Long-Term)

There is a wide range of early and late immune responses to the virus based on the individual’s immune genetics to both direct and indirect viral induced injury and the subsequent development of autoimmunity. I have shown this work with mouse models in the Immunology lab that I led at Johns Hopkins University for a 12-year period. The mechanism of post-viral autoimmunity involves:

  1. molecular mimicry
  2. “innocent bystander” activation of pre-primed autoreactive T-cells
  3. viral persistence

One example of this is in relatively healthy and young individuals who are facing long-term COVID-19 consequences. College athletes have developed myocarditis post-COVID-19, all of whom experienced either mild or asymptomatic infection.

Autoimmunity resulting in long-term pulmonary symptoms is seen in those patients who were more severely ill in hospitalization stays and asymptomatic patients alike. These patients have abnormal chest X-Rays or CT scans and face permanent lung scarring damage (pulmonary fibrosis).

A variety of autoantibodies have been noted in COVID-19 survivors that are broadly reactive, with a wide spectrum effect of targeting the body’s immune system, clotting factors, brain and connective tissue. A study was performed in December 2020 to investigate autoantibody production in COVID-19 patients which suggested the wide range of long-term immune functionality impacts.

It is suggested, and I agree, that many of the “long-haul COVID-19 patients” also have persistent immune regulation problems and are very likely to suffer from an autoimmune component.

Conclusion

Predisposition to COVID-19 autoimmune conditions is either genetic, which we cannot change, or due to our immune systems not being regulated properly. The goal is therefore to optimize the immune response in the most regulated ways possible. Simple solutions may include these every day remedies for overall immune health:

  • Vitamin D, Vitamin C, Vitamin A, Melatonin, Zinc
  • Glutathione, elderberry
  • Omega-3 Fatty Acids

There are of course many others that I have emphasized many times before and are detailed in eMedTalk VII: State-of-the-Art: COVID Pandemic Update.

Disclaimer: This information is formulated as my opinion, and recommend that any individual speak with their primary doctor about their own personal health concerns and questions.

Sources:

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About Ahvie Herskowitz, MD

Dr. Herskowitz’s extensive training includes a medical degree from The Albert Einstein College of Medicine, residencies in Anatomic Pathology and Internal Medicine, and Fellowship training in Cardiology at The Johns Hopkins Medical Center. During his 12 years at Johns Hopkins, he became Associate Professor of Medicine and Immunology and Molecular Microbiology and led a research team in the study of molecular and immunological mechanisms of inflammation, autoimmunity, ischemia, heart transplantation rejection and congestive heart failure.

Dr. Herskowitz’s latest academic appointment was as Clinical Professor of Medicine at UC San Francisco. To learn more about Dr. Herskowitz, you can read it bio here.

      

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