First Study Shows SARS-CoV-2 Induces Long-Lived Memory B Cells That May Provide Lifelong Immunity to COVID-19
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By HospiMedica International staff writers Posted on 30 Sep 2020 |

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New research suggests that past colds may provide some protection from the SARS-CoV-2 virus and that immunity to COVID-19 is likely to last a long time, maybe even a lifetime.
A study by infectious disease experts at the University of Rochester Medical Center (Rochester, NY, USA) is the first to show that 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 that B cells which once attacked cold-causing coronaviruses appeared to also recognize SARS-CoV-2. The researchers believe that 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. These 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 the 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, although one of its components, the S2 subunit, remains similar across all of the viruses. Memory B cells are unable to differentiate between the spike S2 subunits of the different coronaviruses and attack indiscriminately. At least, the study found that was true for beta-coronaviruses, a subclass that includes two cold-causing viruses as well as SARS, MERS and SARS-CoV-2. What the study did not show was the level of protection provided by cross-reactive memory B cells and how it impacts patient outcomes.
“That’s next,” said David Topham, Ph.D., the Marie Curran Wilson and Joseph Chamberlain Wilson Professor of Microbiology and Immunology at URMC, 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.”
Related Links:
University of Rochester Medical Center
A study by infectious disease experts at the University of Rochester Medical Center (Rochester, NY, USA) is the first to show that 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 that B cells which once attacked cold-causing coronaviruses appeared to also recognize SARS-CoV-2. The researchers believe that 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. These 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 the 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, although one of its components, the S2 subunit, remains similar across all of the viruses. Memory B cells are unable to differentiate between the spike S2 subunits of the different coronaviruses and attack indiscriminately. At least, the study found that was true for beta-coronaviruses, a subclass that includes two cold-causing viruses as well as SARS, MERS and SARS-CoV-2. What the study did not show was the level of protection provided by cross-reactive memory B cells and how it impacts patient outcomes.
“That’s next,” said David Topham, Ph.D., the Marie Curran Wilson and Joseph Chamberlain Wilson Professor of Microbiology and Immunology at URMC, 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.”
Related Links:
University of Rochester Medical Center
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