In some cases, the immune system can be prone to amnesia. The body’s memory of the measles virus (or the measles vaccine), for instance, seems to last decades, perhaps an entire lifetime. But the mumps virus appears to make less of a lasting impression.
Researchers aren’t sure why some microbes are more memorable than others, but there are hints. The nature of the initial encounter can influence the immune system’s later reactions. More severe sickness, for example, sometimes goads the body into taking a threat more seriously and locking away information about it long term. (Very severe disease, however, can so thoroughly overwhelm the body that the immune system doesn’t form a good memory of the virus.) Certain bugs might also directly interfere with immune cells’ long-term memory. And factors such as age or biological sex can affect the potency of immune responses as well.
Against respiratory viruses such as the new coronavirus, “people generally have a very strong immune response,” Koelle said. With only about a year’s worth of data, scientists can’t yet confidently forecast how long that protection will last—but a growing body of evidence suggests some serious staying power.
Last summer, researchers in Hong Kong reported the world’s first confirmed coronavirus reinfection, roughly five months after the patient’s initial illness. But his first case had been mild, and his second was symptomless, a fairly unsurprising, perhaps even comforting, trajectory. At the time, many experts floated the notion that the man had not mounted a good enough immune response the first time around—that his body had, on some level, failed him. Since then, dozens of similar cases of milder reinfections have been conclusively documented, and more are suspected.
But consider the other party in this fight. Although the coronavirus mutates more slowly than other respiratory viruses, it still evolves dizzyingly fast. No single genetic change can turn a virus invisible to an entire immune system, but successive shifts in the virus’s appearance can chip away at its familiarity. Subsequent infections under these circumstances are less about the body forgetting, and more about the virus disguising itself—the difference between a robbery abetted by a faulty security system, and one that succeeds because the burglar was in costume.
“From the body’s perspective, that can be a whole different bug,” C. Brandon Ogbunu, a disease ecologist and computational biologist at Yale, told me. Eventually, every evolving virus may change enough that a new infection is no longer a reinfection, but a separate, related one: a sororal infection, or an epi-infection.
These evasion tactics seem to play a role in enabling coronaviruses that cause common colds to infiltrate the human population on a regular basis, says Jesse Bloom, an evolutionary biologist and virologist at the University of Washington. In December, Bloom’s team posted a preprint study detailing the intricate arms race between human and microbe: Antibodies that could successfully squelch one version of a common-cold coronavirus stick around in people for years, but struggle to extinguish its genetically rejiggered descendants.