“Yes, we should be concerned,” Ali Ellebedy, an immunologist at Washington University in St. Louis, told me. “But I think we should also be optimistic.”
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When any infectious interloper hits, the body’s first responders—the less specialized cells of the innate immune system—rush in to wallop it. Those cells also gather information on the invader and ferry it to the lymph nodes, where they parade pieces of the pathogen in front of the body’s longer-term defenders, the cells of the adaptive immune system.
Among these adaptive cells are B cells, each wired to recognize a slightly different hunk of foreign matter. During their development, individual B cells will mix and match segments of genes that encode antibodies, generating billions or trillions of unique combinations. The result is a multitude of Y-shaped molecules that can collectively “respond to any foreign pathogens they see,” says Kim Jacobson, an immunologist at Monash University in Australia. The focus of these antibodies is so laser-sharp that they can differentiate even the individual nooks and crannies that decorate a virus’s surface.
The large majority of B cells won’t be triggered by the chunks of virus shuttled in during any given infection. But the few that are will begin to rapidly copy themselves in hopes of joining the fray. Some will immediately transform into antibody factories, pumping out gobs of the Y-shaped molecules to run rapid viral interference. Others, however, will remain in the lymph nodes to further study the virus.
Here they will split themselves into more B cells, deliberately introducing errors into their genetic code. If the original genetic scramble created antibodies prepared to take on all manner of pathogens, these random but more subtle tweaks have a chance of enhancing the ability to vanquish the specific virus at hand. The process is a bit like evolution on steroids: Mediocrity gets repeatedly weeded out, leaving only the sharpest and strongest killers behind. By the time a virus has vacated the body, the antibodies being produced against it are, on average, more precise and potent.
Much of this painstaking refinement continues after the virus itself is gone: Certain innate cells will cling to scraps of viral corpses—macabre souvenirs of maladies past—to keep the B cells’ boot camp open in the lymph nodes. In a study published last month in the journal Nature, researchers found that the antibodies of COVID-19 survivors continue to strengthen their grip on the coronavirus for several months.
“Over time, our antibodies just become better,” Ellebedy said.
After infection is cleared, most of the B cells that rallied to the fore will die off, their life purpose fulfilled. But some cloister themselves in the bone marrow, eking out small quantities of antibodies. Others—the so-called memory contingent—will drift quietly throughout the body like sentinels, scanning the blood and tissues for trace signals that the same virus has returned to trouble them again. Called back into action, these memory B cells can immediately start pumping out antibodies. Or they can reenter training centers in the lymph nodes to continue their education on the virus, honing their defensive skills further.