Mystery of COVID 19: There is NEW evidence to suggest that COVID 19 is causing the body to make antibodies that attack itself.

COVID 19 is mysterious in a lot of ways, despite us already knowing a lot about it. Researchers & doctors are working hard to unravel the cause and effect of the interaction between the SARS-CoV-2 virus and the immune system. COVID causes several symptoms that may point to a phenomenon called autoimmunity as a potential cause of long COVID. This includes pulmonary fibrosis, meaning scarring of the lungs. Unfortunately, I’m seeing the same picture unfold in so many of my patients who have had COVID, with all this scarring in their lungs. And COVID can cause other issues, like brain changes, skin rashes, excessive blood clotting, inflamed blood vessels, and more.

Autoimmunity is when the immune system mounts an attack on its own healthy cells and tissues—mistaking them for foreign or virally infected cells. Under normal conditions, the immune system can discriminate between self and foreigners. Meaning it can differentiate between the body’s proteins and foreign antigens. But sometimes, in some people, the immune system can mistakenly identify its own proteins as foreign antigens, and it launches its attack on itself. When these autoantibodies react against self-antigens, the outcome can be inflammation and damage to tissues. This is what happens with autoimmune diseases like Type 1 diabetes, Graves’ disease, multiple sclerosis.

The Mystery of COVID 19

This is also what happens with idiopathic pulmonary fibrosis, where people develop scarring in their lungs, much in the same way that this happens with COVID 19. In fact, there are lots of auto-immune conditions that can cause scarring in the lungs, like lupus, rheumatoid arthritis, scleroderma, polymyositis, ankylosing spondylitis, and more—the evidence to support the role of autoantibodies as a cause of more severe COVID 19. The vast majority of people who get COVID 19 will have a disease isolated to the upper respiratory tract. But in 20 percent of people, the infection will go deep into the lung parenchyma and have the potential to cause more severe disease, meaning COVID pneumonia, which sometimes blossoms into ARDS.

Autoimmunity as a potential cause of more severe COVID 19 disease was brought up when autopsies. Cytokine storms are an overreaction by the immune system and are more systemic and short-term. In contrast, autoantibodies are more targeted and long-term. Dexamethasone, a corticosteroid, and the arthritis drugs tocilizumab and sarilumab have been used to modulate an overactive immune response. In a clinical trial, tocilizumab and sarilumab improved critically ill patients’ outcomes on a ventilator in the intensive care unit.

A study at Rockefeller University in New York enrolled almost a thousand people with severe COVID 19. About 10% had antibodies that blocked the action of type 1 interferon molecules, a protein that helps the immune system fight pathogens. These autoantibodies were more common in men, who had 12.5% compared to 2.6% in women. This may explain why men are more likely to have severe disease. Thes are now screening study’s researchers40,000 people to see what proportion of uninfected people carry these antibodies and their distribution by age, ancestry, and gender. This data will be compared to the distribution and percentage of each factor in people with severe COVID 19.

Researchers in another study supported the finding of increased autoantibodies in COVID patients. The antibodies they found were directed towards B cells, a type of immune cell that produces antibodies and interferon. Although the researchers noted no “COVID 19 specific” autoantibodies that distinguish COVID patients from uninfected controls, the levels of autoantibodies were correlated with known markers for inflammation.

The correlations became more extreme as the disease worsened. These medications require careful timing to interrupt an overreactive immune system without interfering with a normal immune system fighting the COVID 19 infection. COVID 19 is often a biphasic illness with an initial phase, primarily respiratory symptoms caused by the virus and the immediate immune response, with innate immunity. Sometimes, it is followed by a secondary inflammatory phase.

There are two immune system arms, the non-specific innate immune system and the specific adaptive immune system. Whenever you are infected with a pathogen that is new to your immune system, you rely on the innate immune system to fight the pathogen. Interferons are essential to the innate response. Interferon-β is one of the first cytokines produced and drives the innate immune response in the lung. This connection illustrates the importance of the finding that SARS-CoV-2 may inhibit interferon activity in those who develop more severe COVID 19.

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine

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