January 29, 2021 – An international team of researchers studying COVID-19 has made a surprising and crucial discovery: the virus appears to induce the body to manufacture weapons to attack its own tissues.
The finding could uncover a number of clinical riddles of COVID. This includes the puzzling collection of symptoms that may be associated with the infection. the persistence of symptoms in some people for months after clearing the virus, a phenomenon known as long-term COVID; and why some children and adults have a severe inflammatory syndrome called MIS-C or MIS-A after their infections.
“It suggests that the virus is directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford University in Stanford, CA.
The study also raises the question of whether other viruses may also affect the body’s tolerance of itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.
Utz says he and his team will next screen flu patients to see if this virus could also cause this phenomenon.
“I assume that it will not only be specific for SARS-CoV-2. I’m willing to bet we’ll find this in other respiratory viruses, ”he says.
The study follows a handful of smaller, more detailed studies that have come to similar conclusions.
The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and one in Germany.
The researchers used blood tests to look at their immune responses as their infections progressed. The researchers looked for autoantibodies – weapons of the immune system that become villains and start an attack on 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 with less than 15% of healthy and uninfected people.
Some people with autoantibodies had little changes over the course of their infections. This suggests that the autoantibodies were there to begin with, which may have caused the infection to spiral out of control in the body.
“Your body is prepared to get bad COVID, and it’s likely caused by the autoantibodies,” says Utz.
In others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting that they were directly related to the viral infection rather than a pre-existing condition.
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 demand reinforcement and can interfere with a virus’ ability to copy itself. Removing them is an effective evasive tactic, and previous studies have shown that people born with genes that cause lower interferon function, or who make autoantibodies to these proteins, appear to be at higher risk of life-threatening COVID infections.
“It seems to give the virus a strong advantage,” says study author John Wherry, PhD, who heads the Department of Immunology at the University of Pennsylvania.
“Now your immune system is staring at Mount Everest instead of climbing a tiny little hill. This is really wrong. “
In addition to those countering the immune system, some people in the study had autoantibodies against muscles and connective tissue, which are common in some rare diseases
Utz said they started the study after seeing COVID patients with strange clusters of symptoms that looked more like autoimmune diseases than viral infections – rashes, joint pain, fatigue, sore muscles, brain swelling, dry eyes, blood that clots easily and blood vessels are inflamed.
“One thing that is very important is that we don’t know whether these patients will continue to develop an autoimmune disease,” says Utz. “I think we’ll be able to answer that question in the next 6 to 12 months if we follow the long-distance riders and examine their samples.”
According to Utz, it will be important to study autoantibodies over long distances to see whether they can precisely identify which ones seem to be at work in the disease. If you can spot them early, you may be able to treat those who are at risk of showing symptoms with drugs that suppress the immune system.
That means, he says, that COVID will be with us for a long time.
“We need to be aware that this virus will cause long-term harm to survivors. Not just the long-distance drivers, but everyone with lung and heart damage and everything else. We will study this virus and its badness for decades, ”says Utz.
sources
BioRxiv, Jan. 29, 2021.
Paul Utz, MD, Professor of Immunology and Rheumatology, Stanford University, Stanford, CA.
John Wherry, PhD, Chairman, Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia.
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