The virus leaves antibodies that can attack healthy tissue; B cell antibodies are weakened, Omicron has not defeated them by Reuters

By Nancy Lapid

(Reuters) – This is a summary of recent research on COVID-19. They include research that requires further research to verify the findings, which is yet to be verified through peer review.

Coronavirus allows survivors of self-attack antibodies

One month after being cured of SARS-CoV-2 infection, survivors have high levels of antibodies that can harm their organs and tissues, even if they are not seriously ill, according to new findings.

Among the 177 health workers who were cured of previously contracted coronavirus infections before the vaccines became available, all had persistent autoantibodies, including chronic inflammation and damage to the joints, skin and nervous system. “We wouldn’t normally expect these people to have elevated multiple sets of autoantibodies or to be elevated for six months after complete clinical healing,” said Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles. Patterns of elevated autoantibodies varied between men and women, the researchers reported in the Journal of Translational Medicine on Thursday.

“We still don’t know how long, over six months, the antibodies will be elevated and / or cause any major clinical symptoms,” Cheng said. “It will be essential to keep track of the people who are moving forward.” His team is investigating whether autoantibody increases are related to the persistent symptoms of people with long-term COVID, and plans to study autoantibody levels after newer variants of the virus after infections.

B cell effects were weakened but were not defeated by Omicron

The researchers believe that the effects of antibodies produced by the immune system’s “memory B cells” against the Omicron variant of coronavirus, although weakened, may still be significant.

When the body learns to recognize SARS-CoV-2 after infection or vaccination, B cells produce fresh antibodies to the virus if they do not circulate enough antibodies to neutralize it in the blood. In a study reported prior to the BioRxiv review, researchers looked at the strength of more than 300 antibodies produced by memory B cells produced by vaccinated volunteers, including some with SARS-CoV-2 infection.

“Omicron appeared to prevent a large chunk of memory B cells,” the researchers said, adding that “30% of all antibodies and close to 10% of all potent neutralizing antibodies still appear to be effectively known,” Matthieu said. Mahevas and Pascal Chappert of the University of Paris in a joint email. Memory B’s strong ability to reproduce and produce antibodies can offset the reduced efficacy of these antibodies in “less than two days,” they have speculated.

Combined with other components of the immune system, especially T cells, the effects of B cells are likely to help explain why most people who become infected are not sick enough to need hospitalization.

It makes the activity of virus variants in cells more efficient

The researchers found that along with peak mutations that help coronaviruses enter cells, mutations that change how the virus behaves within cells are major factors because some variants have become more transmissible.

The findings, published in the journal Nature, show that scientists “need to start studying mutations outside the tip,” which has so far been the main focus of vaccines and antibodies, said Nevan Krogan of the University of California, San Francisco. By studying the Alpha variant, his team found a mutation at a pointless site, which caused the infected cells to increase production of a protein called Orf9B. Orf9b, in turn, disables a protein called TOM70, which cells use to send signals to the immune system. As higher levels of Orf9B disable TOM70, the immune system does not respond well and the virus can better avoid detection, the researchers said.

Referring to the rise in Orf9B, Krogan said: “It’s rare for mutations to ‘turn on’ a protein. It’s a very malicious thing to do with this virus.” The same mutation was identified in the delta, “and probably almost the same mutation is found in Omicron,” he said, suggesting that it may have similar effects on the immune system. The new information could encourage the development of drugs aimed at the interaction of Orf9b and TOM70.

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