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 Coronavirus leaves survivors with self-attacking antibodies
Months after recovering from SARS-CoV-2 infection, survivors have
elevated levels of antibodies that can mistakenly attack their own
organs and tissues, even if they had not been severely ill,
according to new findings.
Among 177 healthcare workers who had recovered from confirmed
coronavirus infections contracted before the availability of
vaccines, all had persistent autoantibodies, including ones that can
cause chronic inflammation and injury of the joints, skin and
nervous system. "We would not normally expect to see such a diverse
array of autoantibodies elevated in these individuals or stay
elevated for as long six months after full clinical recovery," 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 on Thursday in the Journal of
Translational Medicine .
"We don't yet know how much longer, beyond six months, the
antibodies will stay elevated and/or lead to any important clinical
symptoms," Cheng said. "It will be essential to monitor individuals
moving forward." Her team is investigating whether autoantibody
elevations are linked with persistent symptoms in people with long
COVID and planning to study autoantibody levels after infections
with newer variants of the virus.
B cells' effects weakened but not defeated by Omicron
The effects of antibodies produced by the immune system's "memory B
cells" against the Omicron variant of the coronavirus, while
weakened, could still be significant, researchers believe.
Once the body learns to recognize SARS-CoV-2, either after infection
or vaccination, B cells generate fresh antibodies against the virus
if there are not already enough antibodies circulating in the blood
that can neutralize it. In a study reported on bioRxiv ahead of peer
review, researchers analyzed the strength of more than 300
antibodies produced by memory B cells obtained from vaccinated
volunteers, including some who had a prior SARS-CoV-2 infection.
"Omicron seemed to evade a very large share of the memory B cells
pool," researchers said, adding that it "seems to still be
efficiently recognized by 30% of total antibodies and close to 10%
of all potent neutralizing antibodies," said Matthieu Mahevas and
Pascal Chappert of Universite de Paris in a joint email. Memory B
cells' robust ability to proliferate and produce antibodies might
compensate "in less than two days" for those antibodies' reduced
effectiveness, they speculate.
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 In combination with other
immune system components, particularly T cells,
the effects of B cells likely help to explain
why most vaccinated individuals who become
infected do not become sick enough to require
hospitalization, they said.
Virus variants' activity in cells makes them more effective
Along with spike mutations that help the coronavirus break into
cells, mutations that change how the virus behaves inside the cells
are a big factor in why some variants have been more transmissible,
researchers have discovered.
The findings, published in Nature, show that scientists "have to
start looking at mutations outside the spike," which has so far been
the main focus of vaccines and antibody drugs, said Nevan Krogan of
the University of California, San Francisco. Studying the Alpha
variant, his team found a mutation at a non-spike site that causes
infected cells to ramp up their production of a protein called
Orf9B. Orf9b in turn disables a protein called TOM70 that cells use
to send signals to the immune system. With higher levels of Orf9B
disabling TOM70, the immune system does not respond as well and the
virus can better evade detection, the researchers said.
Referring to the increase in Orf9B, Krogan said, "It's rare that
mutations 'turn up' a protein. It's a very sneaky thing for this
virus to do." The same mutation was identified on Delta, "and sure
enough, almost the same mutation is on Omicron," he said, which
suggests they may have similar effects on the immune system. The new
information could spur development of drugs that target the
interaction of Orf9b and TOM70.
Click for a Reuters graphic https://tmsnrt.rs/3c7R3Bl on vaccines in
development.
(Reporting by Nancy Lapid; Editing by Bill Berkrot)
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