The seasonal colds you’ve had in the past may provide some protection from COVID-19, researchers report.
The new study also suggests that immunity to COVID-19 is likely to last a long time—maybe even a lifetime.
The study in mBio is the first to show that the COVID-19-causing virus, SARS-CoV-2, induces memory B cells, long-lived immune cells that detect pathogens, create antibodies to destroy them, and remember them for the future.
The next time that pathogen tries to enter the body, those memory B cells can hop into action even faster to clear the infection before it starts.
Because memory B cells can survive for decades, they could protect COVID-19 survivors from subsequent infections for a long time, but further research will have to bear that out.
The study is also the first to report cross-reactivity of memory B cells—meaning B cells that once attacked cold-causing coronaviruses appeared to also recognize SARS-CoV-2. The researchers believe this could mean that anyone who has been infected by a common coronavirus—which is nearly everyone— may have some degree of pre-existing immunity to COVID-19.
“When we looked at blood samples from people who were recovering from COVID-19, it looked like many of them had a pre-existing pool of memory B cells that could recognize SARS-CoV-2 and rapidly produce antibodies that could attack it,” says lead author Mark Sangster, a research professor of microbiology and immunology at the University of Rochester Medical Center.
The findings are based on a comparison of blood samples from 26 people who were recovering from mild to moderate COVID-19 and 21 healthy donors whose samples were collected six to 10 years ago—long before they could have been exposed to COVID-19.
From those samples, the researchers measured levels of memory B cells and antibodies that target specific parts of the spike protein, which exists in all coronaviruses and is crucial for helping the viruses infect cells.
The spike protein looks and acts a little different in each coronavirus, but one of its components, the S2 subunit, stays pretty much the same across all of the viruses. Memory B cells can’t tell the difference between the spike S2 subunits of the different coronaviruses and attack indiscriminately. At least, the study shows that was true for beta-coronaviruses, a subclass that includes two cold-causing viruses as well as SARS, MERS, and SARS-CoV-2.
What this study doesn’t show is the level of protection provided by cross-reactive memory B cells and how it impacts patient outcomes.
“That’s next,” says David Topham, a professor of microbiology and immunology who runs the lab that conducted this work.
“Now we need to see if having this pool of pre-existing memory B cells correlates with milder symptoms and shorter disease course—or if it helps boost the effectiveness of COVID-19 vaccines,” he says.
Source: University of Rochester
