The SARS-CoV-2 virus shares an important feature with some viruses that cause the common cold, and the structural similarity suggests that people with a history of the common cold may carry some immunity against SARS-CoV-2 infection, new evidence reveals.
Infection with SARS-CoV-2 also boosts production of memory B cells, long-lasting components of immune protection. Even though antibodies to SARS-CoV-2 tend to wane over time, these memory B cells lie in wait and could mount a quick defense should re-infection occur, researchers report in a study published online September 25 in the journal mBio, a publication of the American Society for Microbiology.
“Much of the discussion about our study has focused on our evidence that memory B cells generated by human infection with common cold coronaviruses are cross-reactive with SARS-CoV-2 and produce antibodies in response to SARS-CoV-2 infection,”.
“Perhaps most importantly, these memory B cells recognize the conserved S2 region of the SARS-CoV-2 spike protein and produce anti-S2 antibodies,” said Sangster, research professor at the David H. Smith Center for Vaccine Biology and Immunology, University of Rochester Medical Center, Rochester, New York.
Just how much immune protection these anti-S2 antibodies confer against COVID-19, however, remains unknown.
Searching for Similarities
Of the four endemic virus strains linked to the common cold, two are betacoronaviruses. Because SARS-CoV-2 is in the same family of viruses, researchers initially searched for shared key structural proteins. However, early studies did not yield evidence of substantial cross-reactivity.
More recently, however, multiple investigators report finding relevant B- and T-cell immunity in people without COVID-19 that could offer some degree of future protection against SARS-CoV-2.
Building on these findings, Sangster, senior coauthor David J. Topham, PhD, and colleagues compared 26 nonhospitalized, convalescent COVID-19 patients with a group of 20 healthcare workers without a COVID-19 diagnosis at Strong Memorial Hospital in Rochester and another cohort of 21 healthy adults assessed before the pandemic.
One link to the common cold viruses was the finding that immunoglobulin G or “IgG reactive to the S2 was widespread in unexposed subjects and likely resulted from exposure to human coronaviruses,” the researchers write.
This discovery could help explain the wide spectrum of COVID-19 severity, Sangster said. “The clearest and most important takeaway message from our work is that SARS-CoV-2 infection generates and/or expands memory B cell populations that recognize SARS-CoV-2 proteins.”
Memory B cells mediate the secondary antibody response that is characterized by rapid production of large amounts of high-affinity antiviral antibodies, Sangster said. “It is also well established that memory B-cell populations are maintained for many years, perhaps decades.”