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Survivors of Covid-19 Were Shown to Have Higher Levels of Self-attacking Antibodies.


People who contracted and recovered from COVID-19 may have generated antibodies that could harm their organs and tissues in the long run, according to new research.

It has recently been discovered that SARS-CoV-2 infection can lead to an immune response involving self-destructive antibodies that can linger for months beyond the initial infection and recovery.

Reactivity of Antibodies to the Self

A team of researchers studied the autoantibody reactivity of 117 people for the study (65 percent women, 35 percent men, the mean age of 35). All of them had previously been infected with SARS-CoV-2. 53 healthy pre-pandemic individuals were used as comparisons for the study’s results.

Survivors of Covid-19 Were Shown to Have Higher Levels of Self-attacking Antibodies.

Autoantibody reactivity was more evident in women with an asymptomatic infection and in men with a mild symptomatic infection after considering all of the data. In the absence of a serious illness, individuals nonetheless produced a wide autoantibody response, according to the researchers.

As part of the study, Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles told Reuters, “We would not ordinarily anticipate to observe such a varied array of autoantibodies high in these individuals or stay up for as long six months after full clinical recovery.”

Autoantibodies’ Long-Term Retention

Before starting the trial, the researchers already knew that a serious infection might trigger the immune system to manufacture large numbers of autoantibodies. Autoantibodies were triggered regardless of how mild or severe the infection was.

This discovery astonished the researchers during their study. Among their many accomplishments, they include being the first to document the long-term persistence of the autoantibodies.


If the antibodies remain elevated and/or cause any significant clinical effects beyond six months, we don’t yet know.” In the future, it will be critical to keeping an eye on individuals,” Cheng noted.

As co-senior author and research scientist in the Cardiology Department at the Smidt Heart Institute, Justyna Fert-Bober, Ph.D. said their findings could help explain “long COVID.”

What makes COVID-19 so unique is explained by these discoveries. In those who go on to acquire a syndrome now known as long COVID-19, these patterns of immune dysregulation may underlie the various sorts of persistent symptoms we witness. Fert-Bober was quoted by Science Daily as saying:

In the Journal of Translational Medicine, Cedars-Sinai researchers reported their findings.

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