It seems that with autoinflammatory and autoimmune diseases, COVID-19 shares a common immune system reaction, experts say.
Researchers, whose report is reported in the Journal of Immunology, show that SARS-CoV-2 can trigger the body's immune system to erroneously attack its own cells and tissues in the heart, brain, and elsewhere.
Autoimmunity, they say, can clarify how the virus causes such severe and unpredictable harm. The secret to mitigating the harm and preserving lives might be to consider these autoimmune mechanisms.
STAMFORD, CONNECTICUT - APRIL 24: (EDITORIAL USE ONLY) A "prone team," wearing personal protective equipment (PPE), prepares to turn a COVID-19 patient onto his stomach in a Stamford Hospital intensive care unit (ICU) on April 24, 2020, in Stamford, Connecticut.
The argument for autoimmune inclusion
Experts investigated the function of antibody cells and immune cells in people with extreme COVID-19 in a report in Nature Immunology in October. Any striking parallels to autoimmune disorders have been identified.
Ignacio Sanz, MD, co-author of the report and director of Emory University's Lowance Centre for Human Immunology, said the team found the same form of behavior of B cells we see in lupus flares and related activity of antibodies as well.
Sanz also examined the immune systems of persons with moderate to long-haul COVID-19 cases. Again, he sees the autoimmune diseases converge.
It is probable, Sanz claims that the symptoms he has noted are merely signs of an active immune reaction to an invading organism. But he says that autoimmunity features are highly involved in the production of extreme COVID-19 in at least a sub-group of patients.
Why does the coronavirus induce the immune system to invade its own tissues and cells wrongly? Some of it could have to do with what is considered molecular mimicry by biologists.
A cardiothoracic surgeon and author of a recent report on the autoimmunity components of COVID-19, Timothy Icenogle, MD, observed a variety of parallels between the coronavirus protein amino acid sequences and those of specific proteins.
Icenogle, whose research is reported in Frontiers in Immunology, said these protein comparisons might mislead the immune system and lead it to invade healthy cells on its own. This assault can persist in some persons, even after the real virus cells were washed out.
Autoimmunity could clarify why a strong immune response to the virus does not often equate with mild COVID-19, one that requires the development of coronavirus-neutralizing antibodies.
In certain patients, an antibody reaction developed to kill the virus may wind up destroying healthy cells as well. This autoimmune phenomenon may also clarify why a person gets myocarditis and other types of inflammation or injury months after recovering from COVID-19.
Not quite the whole narrative
The researchers did not observe any COVID-specific autoantibodies to identify seriously ill COVID patients, while COVID patients had several autoantibodies that attacked immune system proteins. What decides when an individual will suffer from extreme COVID is based on several factors, and the whole story is not about autoantibodies.
However, the analysis indicates that persons with known autoantibodies could be at increased risk of developing extreme COVID. During early coronavirus infection, these individuals could have defects in their immune system or are predisposed to making new autoantibodies that may inhibit their immune response to the virus.
The correlation between extreme COVID and misled immune responses aiming at the healthy tissues and proteins in the body is increasingly the focus of researchers. The existence of autoantibodies indicates that COVID may be a coronavirus-induced autoimmune disorder for certain patients. It will allow scientists to create alternative therapies for this disease by recognizing what causes autoantibodies development.
After the infection has healed, scientists do not know how long these autoantibodies last. A significant unresolved question is whether long-term harm induced by autoantibodies could explain any effects of long-term COVID.
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