COVID Virus May Prompt Body to Attack Itself

January 29, 2021 – An international team of researchers studying COVID-19 have made a surprising and crucial discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The discovery could reveal a number of clinical mysteries of COVID. They include the confusing collection of symptoms that can accompany infection; the persistence of symptoms in some people for months after clearing the virus, a phenomenon called long COVID; and why some children and adults have a severe inflammatory syndrome, called MIS-C or MIS-A, after their infections.

“This suggests that the virus could directly cause autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at the University. from Stanford to Stanford, California.

The study also opens the question of whether other viruses could also break the body’s tolerance to itself, causing autoimmune diseases like multiple sclerosis, rheumatoid arthritis and lupus later in life.

Utz says he and his team will then study patients with influenza to see if this virus could cause this phenomenon as well.

“My prediction is that this will not be specific to SARS-CoV-2. I’m willing to bet we’ll find that with other respiratory viruses, ”he says.

The study follows a handful of smaller, detailed surveys that came to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

The researchers used blood tests to study their immune responses as their infections progressed. Researchers have been looking for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies to those found in people who were not infected with the virus that causes COVID.

As previous studies have shown, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared to less than 15% of those who were healthy and uninfected.

Some people with autoantibodies changed little as their infections progressed. This suggests that the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Utz says.

But in others, about 20% of people who had them, autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a condition. pre-existing.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, such as interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Eliminating them is a powerful evasive tactic, and previous studies have shown that people born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk of infections. Life-threatening COVID. .

“This appears to give the virus a powerful advantage,” says study author John Wherry, PhD, who heads the Institute of Immunology at the University of Pennsylvania.

“Now your immune system, instead of having a tiny little hill to climb, is looking at Mount Everest. It’s really devious.

In addition to those that counterattack the immune system, some people in the study had autoantibodies against muscle and connective tissue that are seen in some rare disorders.

Utz says they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – rashes, joint pain, fatigue, muscle pain, swelling of the brain, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that is very important to note is that we don’t know if these patients will develop autoimmune disease,” Utz says. “I think we’ll be able to answer this question in the next 6 to 12 months by tracking long-haul carriers and studying their samples.”

Utz says it will be important to study autoantibodies in long-range carriers to see if they can identify exactly which ones appear to be at work with the disease. If you can catch them early, it might be possible to treat people at risk for persistent symptoms with drugs that suppress the immune system.

What that means, he says, is that COVID will be with us for a long, long time.

“We have to realize that this virus will cause long-term damage to survivors. Not just the long haulers, but all the people with lung damage and heart damage and everything in between. We will be studying this virus and its nastiness for decades, ”says Utz.


BioRxiv, January 29, 2021.

Paul Utz, MD, professor, immunology and rheumatology, Stanford University, Stanford, CA.

John Wherry, PhD, chair, Department of Systems Pharmacology and Translational Therapy, University of Pennsylvania, Philadelphia.

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