Virus leaves antibodies that may attack healthy tissues; B cell antibodies weakened, not defeated by omicron

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

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 recognise 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 neutralise it. In a study reported on bioRxiv ahead of peer
review, researchers analysed 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.

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“Omicron seemed to evade a very large
share of the memory B cells pool,” researchers said, adding that it
“seems to still be efficiently recognised by 30% of total antibodies and
close to 10% of all potent neutralising 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

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 hospitalisation, 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.

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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.

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