Views: 0 Author: Site Editor Publish Time: 2022-01-18 Origin: Site
According to researchers at Cedar Mount Sinai Medical Center, infection with the virus that causes COVID-19 can trigger an immune response that lasts far longer than the initial infection and recovery - even in people with mild or no symptoms at all. The results were published in the Journal of translational medicine.
To conduct their research, the research team at Cedar Mount Sinai Medical Center recruited 177 people who were confirmed to have previously been infected with sars-cov-2. They compared blood samples from these people with samples from healthy people before the pandemic. All people confirmed to be infected with sars-cov-2 had elevated autoantibody levels. Some autoantibodies are also found in people with diseases in which the immune system attacks their own healthy cells, such as lupus erythematosus and rheumatoid arthritis.
Susan Cheng, director of the Institute of healthy aging in the Department of Cardiology at the SMIT Heart Institute and co-author of the study, said: " We have found autoantibody activity signals commonly associated with chronic inflammation and injury involving specific organ systems and tissues, such as joints, skin and nervous system."
Some autoantibodies are associated with autoimmune diseases that usually affect more women than men. However, in this study, the number of autoantibodies increased in men than in women.
"On the one hand, this finding is contradictory given that autoimmune diseases are usually more common in women. On the other hand, this is also expected to some extent given that we know that men are more vulnerable to the most serious form of COVID-19," fert Bober said.
The research team is interested in expanding the scope of the study to find the types of autoantibodies that may exist and persist in people with long-term COVID-19 symptoms. Because this study is aimed at infected people before the emergence of the vaccine, the researchers will also examine whether autoantibodies have similar production in people with breakthrough infection.
"If we can better understand these autoantibody responses and how sars-cov-2 infection triggers and drives these variable responses, we can be closer to determining treatment methods and even preventing these effects from occurring in high-risk groups," Susan said
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