Eight months ago, the new coronavirus was unknown. But to some of our immune cells, the virus was already something of a familiar foe.
A flurry of recent studies has revealed that a large proportion of the population — 20% to 50% of people in some places — might harbor immunity assassins called T cells that recognize the new coronavirus despite having never encountered it before.
These T cells, which lurked in the bloodstreams of people long before the pandemic began, are most likely stragglers from past scuffles with other related coronaviruses, including four that frequently cause common colds. It's a case of family resemblance: In the eyes of the immune system, germs with common roots can look alike, such that when a cousin comes to call, the body may already have an inkling of its intentions.
The presence of these T cells has intrigued experts, who said it was too soon to tell whether the cells would play a helpful, harmful or entirely negligible role in the world's fight against the current coronavirus. But should these so-called cross-reactive T cells exert even a modest influence on the body's immune response to the new coronavirus, they might make the disease milder — and perhaps partly explain why some people who catch the germ become very sick, while others are dealt only a glancing blow.
"If you have a population of T cells that are armed and ready to protect you, you could control the infection better than someone who doesn't have those cross-reactive cells," said Marion Pepper, an immunologist at the University of Washington who is studying the immune responses of COVID-19 patients. "That's what we're all hoping for."
T cells are an exceptionally picky bunch. Each spends the entirety of its life waiting for a very specific trigger, like a hunk of a dangerous virus. Once that switch is flipped, the T cell will clone itself into an army of specialized soldiers, all with their sights set on the same target. Some T cells are microscopic assassins, tailor-made to home in on and destroy infected cells; others coax immune cells called B cells into producing virus-attacking antibodies.
The first time a virus infects the body, this response is sluggish; it takes several days for the immune system to sort out which T cells are best suited for the job at hand. But subsequent encounters typically prompt a response that is stronger and faster, thanks to a reserve force of T cells, called memory T cells, that lingers after the initial threat has passed and can quickly be called into action again.
Usually, this process operates best when T cells must battle the same pathogen again and again. But these recruits are more flexible than they are often given credit for, said Laura Su, an immunologist and T cell expert at the University of Pennsylvania. Should these cells chance upon something that bears a strong resemblance to their germ of choice, they can still be roused to fight, even if the invader is a total newcomer.
In theory, cross-reactive T cells can "protect almost like a vaccine," said Smita Iyer, an immunologist at the University of California, Davis. Previous studies have shown that cross-reactive T cells may guard people against different strains of the flu virus, and perhaps confer a trace of immunity against dengue and Zika viruses, which share a family tree.