In epic tales of the immune system, B cells and their antibodies tend to hog the limelight. Antibodies, which are proteins that drift through the blood, are easy to capture and measure; they’re sometimes powerful enough to waylay a virus before it has the chance to break into a cell. But no antibodies would be produced without the help of T cells, which coax B cells into maturing and play vital roles in their training regimen—loyal wingmen at the ready. T cells are also formidable foes in their own right, capable of recognizing virus-infected cells and forcing them to self-destruct.
T cells don’t undergo the same supercharged mutation process that their B-cell colleagues do. They are stuck with the pathogen sensors they’re born with. But the starting repertoire of T cells, and the number of bugs they can recognize, is similarly massive. And like their B-cell counterparts, T cells are capable of remembering past pathogenic encounters—and their discerning gaze is especially difficult to elude.
When viruses undergo a substantial costume change, it can disrupt this iterative process. It’s a big part of why flu vaccines have to be updated every year, Ellebedy said: “We are always trying to catch up with the virus.”
But coronaviruses mutate far more slowly than flu viruses do. And this new one has yet to undergo a makeover that fully neuters the vaccines we’ve developed against it. “I think there’s probably a very small probability that there will be complete escape,” David Masopust, an immunologist at the University of Minnesota, told me.
B cells and T cells develop so many unique ways of recognizing a given virus that any one mutation, or even a handful, won’t fully thwart them. A change to the equivalent of a virus’s elbow, for example, will have little impact on a T cell’s ability to recognize its earlobe. Memory cells will rapidly seize upon commonalities between the two versions of the virus; in some people, this alone could be enough to nip an infection in the bud.
Certain memory cells—especially T cells—might have enough flexibility to recognize a modified version of their viral target. Experts call this “cross-reactivity,” and it’s a crucial part of the T cell way of life, Laura Su, an immunologist at the University of Pennsylvania, told me. Some scientists have hypothesized that T cells previously marshaled against other coronaviruses, such as those that cause common colds, might even play a small role in quelling this new one.
Even in the complete absence of memory and cross-reactivity, the body still has a huge reserve of backup cells—the multitude of B and T cells that were not triggered by the first go-round with the virus, Su said. The war against variants is not a fight just for veterans: Chances are, rookies are waiting in the lymph nodes to be called to the front lines. Depending on the extent of the virus’s metamorphosis, another infection, perhaps another illness, may be possible. But the body is not left wholly defenseless.