BEST SHOT AGAINST OMICRON-T CELLS

Killer T cells, as their name might imply, are not known for their mercy. When these immunological assassins happen upon a cell that’s been hijacked by a virus, their first instinct is to butcher. The killer T punches holes in the compromised cell and pumps in toxins to destroy it from the inside out. The cell shrinks and collapses; its perforated surface erupts in bubbles and boils, which slough away until little is left but fragmentary mush. The cell dies spectacularly, horrifically—but so, too, do the virus particles inside, and the killer T moves on, eager to murder again.

But  more importantly where antibodies stumble, killer Ts shine. Their entire raison d’être is rooting out infected cells—not free-floating viruses—and they manage that feat through an affinity for gore. As a signal of distress, infected cells can chop up some of the viruses they’re being forced to produce and display the mangled pieces on their outside. The dismembered bits are gross but effective: Nothing makes killer Ts go wild more than a hunk of mutilated virus splattered onto the surface of an infected cell.

T cells become even more important if antibodies are not working well. Cellular infections might start to roll out at a rapid clip, but T cells can swoop in to help corral the pathogen in place, typically within a couple of days. This rapid walling-off can halt the progression of disease, and maybe even curb transmission; it also buys the rest of the immune system time to gather its wits. B cells, reawakened from their slumber, will start to churn out more antibodies to replace the ones that have faded; another group of T cells, nicknamed the helpers, will arrive to help coordinate the rest of the immune response. Getting a booster, too, could jump-start this process ahead of infection, coaxing out extra antibodies and possibly tickling more T cells into joining the fray.

All of this is likely to mean that more vaccinated people could get infected by Omicron—a new and unfortunate hurdle, as the world continues its struggle to contain the super-transmissible Delta. But the immunized will probably still be at much lower risk of getting seriously sick than their unvaccinated peers, a pattern that early studies out of South Africa seem to fit. That’s in keeping with the stepwise fashion in which immune protection tends to ebb: The safeguards against infection—mostly neutralizing antibodies—fall first. But protection against severe disease and death is the last to go; to engineer those very serious outcomes, viruses have to linger in the body, repeatedly thwarting the many defenders that the immune system tosses their way.

But our shot-trained T cells can’t be expected to stand their ground forever. Too many people around the world remain unvaccinated, offering the virus many more chances to splinter into new, troublesome lineages. The quicker the virus moves to colonize us, the more likely it is to outpace our defenses. SARS-CoV-2 could eventually learn to hopscotch over more killer Ts, too—a risk we run when we force our bodies to repeatedly tussle with this fast-changing foe.