The virus leaves antibodies that can attack healthy tissues; B-cell antibodies are impaired, Omicron did not beat them

Author: Nancy Lapid

(Reuters) – The following is a summary of some recent COVID-19 studies. These include research that requires further research to confirm the results and has not yet validated the peer review.

The coronavirus leaves self-attacking antibodies on survivors

Months after recovery from SARS-CoV-2 infection, survivors have elevated levels of antibodies that can accidentally attack their own organs and tissues, even if they were not severely ill, according to new findings.

Of the 177 health care workers who had recovered from confirmed coronavirus infections before the vaccines became available, all had persistent autoantibodies, including those that can cause chronic inflammation and injuries to the joints, skin, and nervous system. “We would not normally expect to see such a diverse set of autoantibodies elevated in these individuals or remain elevated for another six months after complete clinical recovery,” said Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles. Models of elevated autoantibodies varied between men and women, the researchers reported in the Journal of Translational Medicine on Thursday.

Video: Research shows that silver lining may have immunity to omicron

“We don’t yet know how long, more than six months, the antibodies will remain elevated and / or lead to important clinical symptoms,” Cheng said. “It’s important to monitor the progress of individuals.” His team is investigating whether increases in autoantibodies are associated with persistent symptoms in people with long-term COVID virus, and plans to investigate levels of autoantibodies following infections with newer variants of the virus.

Omicron attenuated the effects of B cells but did not overcome them

The researchers believe that the effects of antibodies produced by the “memory B cells” of the immune system against the Omicron variant of coronavirus may be reduced.

As the body learns to recognize SARS-CoV-2, either after infection or vaccination, B cells produce new antibodies to the virus if there are not enough antibodies in the blood to neutralize it. In the BioRxiv study, before the peer review, the researchers analyzed the strength of more than 300 antibodies produced using memory B cells from vaccinated volunteers, including some with previous SARS-CoV-2 infection.

“Omicron seemed to circulate a very large portion of the B-cell pool of B-memory,” the researchers said, adding that “30% of all antibodies and nearly 10% of all effective neutralizing antibodies still seem to recognize it effectively,” said Matthieu. Mahevas and Pascal Chappert from the Universite de Paris in a joint email. They speculate that the strong ability of memory B cells to proliferate and produce antibodies may compensate for the reduced efficacy of these antibodies in “less than two days.”

Together with other components of the immune system, particularly T cells, the effects of B cells are likely to help explain why most vaccinated individuals who become infected do not get enough to require hospitalization, they said.

The activity of virus variants in cells makes them more effective

Together with spike mutations that help the coronavirus break into cells, mutations that change the behavior of the virus within cells are a major factor in why some variants have been more contagious, researchers have found.

Findings published in the journal Nature show that researchers “need to start looking at mutations outside the peak,” which has so far been the main focus of vaccines and antibody drugs, said Nevan Krogan of the University of California at San Francisco. While studying the alpha variant, his team found a mutation in the non-peak that causes infected cells to increase their production of a protein called Orf9B. Orf9b, on the other hand, disables a protein called TOM70, which is used by cells to send signals to the immune system. Higher levels of Orf9B inhibit TOM70, the immune system does not respond as well, and the virus can better avoid detection, the researchers said.

Referring to the increase in Orf9B, Krogan said, “It’s rare for mutations to ‘form’ a protein. It’s very strong for this virus.” The same mutation was identified in Delta, “and certainly almost the same mutation is in Omicron,” he said, suggesting that they may have similar effects on the immune system. The new data may encourage the development of drugs that target the interaction between Orf9b and TOM70.

Click on the Reuters graphic for vaccines under development.

(Reported by Nancy Lapid; edited by Bill Berkrot)

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