In addition, researchers looked for markers of autoimmunity in a larger group of COVID-19 ICU patients and outpatients, comparing them to people who were in intensive care because of bacterial pneumonia. They explored in detail what COVID-19-generated autoantibodies react against, both during acute infection and later. Eun-Hyung Lee, MD, isolated thousands of antibody-secreting cells from seven COVID-19 patients who were in intensive care units (ICUs) at Emory hospitals. In the Nature paper, researchers led by Ignacio Sanz, MD, and F. This finding may influence scientific understanding of post-viral chronic illnesses more broadly. In addition, therapies that deplete autoantibody activity may improve longer-term recovery outcomes, the Emory investigators suggest.Ĭritically, high levels of autoantibodies were also observed in hospitalized patients with bacterial pneumonia, suggesting the triggering of autoimmunity is not limited to SARS-CoV-2 infection and occurs in other settings during intense inflammation. One type of antibody (against carbamylated proteins) seems to closely correlate with overall autoimmunity. Testing for autoantibodies during acute infection may enable identification of some patients who need early intervention to head off problems later. Follow-up studies are now underway to understand just how long these misdirected immune responses may last.
Often the situation will eventually resolve and cause no further disease.”įor a moderate number of people with long COVID -about one third -their levels of some types of autoantibodies fall but remain elevated above normal for months after the initial infection. “It temporarily loses sight of the viral target and produces self-targeting antibodies. “The immune system can make mistakes under duress,” says Emory immunologist Matthew Woodruff, PhD, who is co-first author of the paper. This was the case for most hospitalized patients who then recovered. However, after the storm passes, the autoantibodies decay and are mostly removed from the body over time.
#COVID RASH IMAGES SKIN#
It appears that during a severe COVID-19 infection, the immune system sabotages itself by generating a wide variety of autoantibodies: proteins that are usually tools for defense, but in this situation, attack the body’s own tissues.ĭuring acute infection, COVID-19 patients’ immune systems resemble those of people with diseases such as lupus or rheumatoid arthritis, for whom autoantibodies contribute to symptoms such as fatigue, skin rashes and joint pain. New findings on COVID-19-triggered autoimmunity have implications for both the treatment of acute infection and for people with long COVID, in which self-targeted antibodies have emerged as a key characteristic.
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