Read: The body is far from helpless against coronavirus variants.
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.
“It makes perfect sense—it’s what viruses do,” Oliver Fregoso, a virologist at UCLA, says. “Viruses are going to evolve in a way that [allows] them to continue infecting. Otherwise, they go extinct.”
No part of reinfection is cut-and-dried. Every infection, foreign or familiar, to some extent, reflects the push and pull between immunity and viral evolution—both of which can make a once-familiar foe appear foreign. Unfortunately, “it’s hard to parse out how much is due to you, as the patient, versus the characteristics of the virus,” Bloom says. The majority of people infected by the coronavirus don’t get the chance to measure their immune response, or genetically sequence the virus infecting them, which would be a surefire way to tell whether the pathogen has morphed into something new.
But the more we understand about how these dynamics work, the better equipped we’ll be to tinker with them—and give our own bodies the edge. “We have to be able to explain when things don’t go right,” Ogbunu said. Scientists might be able to more effectively tailor treatments, some perhaps more suited to people with weaker immune systems, others hyper-focused on foiling certain variants of the virus. The same intel could inform the production and distribution of vaccines, which could be reformulated to get ahead of new variants. Understanding the root of most coronavirus reinfections is about prioritizing what’s in our pandemic playbook: shoring up our defense, or hitting the virus hard with the best offense we’ve got.
Sarah Cobey, an immunologist at the University of Chicago, says the past year hasn’t shaken her faith in the human immune system. Some rare individuals have gotten very ill the second time they’ve been infected, a few even sicker than the first. But failed or aberrant immunity to the coronavirus is unlikely to be the norm. Most of the reinfections we document going forward will probably involve the virus adopting a new and foreign guise, Cobey says, rather than “something really weird happening with immune memory.”
Read: A simple rule of thumb for knowing when the pandemic is over.
In many ways, the virus-shift version of repeat infections is the easier one. It’s expected and trackable, with testing and genomic surveillance; it’s haltable, with measures that keep the virus from spreading and lingering in hosts. Encouragingly, none of the variants yet seems capable of completely eluding a typical immune response to the OG coronavirus or an OG-based vaccine—which is also very good news. It’s a hint that, by and large, our immune systems are working as they should. The shots we’ve developed to protect us from the coronavirus will still dial down our risks of getting seriously sick with COVID-19; vaccine makers will update their recipes to account for the variants. People who are hit naturally with one variant, then another, will probably experience gentler symptoms the second time, if they feel ill at all. (Frequent, symptomatic reinfections with the same variant, by contrast, would forecast a less rosy future.)
