Coronavirus Reinfection Will Soon Become Our Reality

a lung overlaid with silhouettes of the coronavirus
Adam Maida / Getty / The Atlantic

On its face, reinfection appears to be a straightforward term. It is literally “infection, again”—a recovered person’s second dalliance with the same microbe. Long written into the scientific literature of infectious disease, it is a familiar word, innocuous enough: a microbial echo, an immunological encore act.

But thanks to the pandemic, reinfection has become a semantic and scientific mess.

Newly saddled with the baggage of COVID-19, reinfection has taken on a more terrifying aspect, raising the specter of never-ending cycles of disease. It has sat at the center of debates over testing, immunity, and vaccines; its meaning muddled by ominous headlines, it has become wildly misunderstood. When I ask immunologists about reinfection in the context of the coronavirus, many sigh.

I don’t blame them. At the heart of any conversation about reinfection is a largely unsolved mystery: whether COVID-19 survivors are truly safe from the coronavirus. Last summer, a cluster of apparent cases of reinfection seemed to hint that the virus was stronger than the body’s ability to protect against it—that reinfection, though uncommon, could be chalked up to a failure of the body’s defenses.

But infection is a two-player game, and a change in either contender can affect the dynamics of a second confrontation. On occasion, the body’s immune strongholds might weaken and crack. Or a microbe might alter its surface until it’s unrecognizable to the host that once fought it off—even if the original defenses raised against the bug are still standing tall. These latter cases might be described less strictly as reinfection than as, well, another infection.

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As the coronavirus continues to mutate—a process hastened by the sheer number of hosts that the virus has found around the globe—cases such as these might soon become our startling reality. For most of 2020, there was only one widely recognized coronavirus variant of consequence—the OG SARS-CoV-2, if you will. Recently, researchers have identified several instances in which new variants have set up shop in COVID-19 survivors. Experts haven’t yet settled on common terms to describe these incidents, or distinguish them from cases in which people’s immune defenses have simply dropped.

But untangling how and why the coronavirus reestablishes itself in certain people is essential to preventing that from happening. Understanding reinfection will affect how we develop vaccines and treatments, and monitor the virus’s movements in the future. It could help us figure out how durable immunity to the coronavirus truly is, and the limits of the virus’s capacity to change.


To understand reinfection, it’s helpful to first get a grip on plain old infection. As Brianne Barker, an immunologist at Drew University, explains it, infection fundamentally represents an interaction between a microbe and a host: The bug establishes itself in a living home, where it can reproduce.

Some infections are noisy. They come with the signs and symptoms of illness, either because the pathogen is causing a ruckus, or because the body has grown cantankerous in its effort to evict an unwelcome tenant. Other microbes are silent houseguests, so unobtrusive that we don’t even notice them. Coronavirus infections seem capable of running the gamut. A person’s infection status can’t tell you whether they can spread the microbe, either. “You can be infected without being infectious,” Katia Koelle, a virologist at Emory University, told me.

The same rules of the road apply to reinfection. A repeat infection won’t necessarily come with the same symptoms, or the same level of contagiousness. In the most classical portrait of reinfection, the microbe is effectively identical; your body, with its memory of the bug, is not. That probably means you’re not “completely susceptible again,” says Angela Rasmussen, a virologist affiliated with Georgetown University.

Typically, a person’s second rendezvous with a pathogen will be much milder, and pose less of a transmission threat. Immune cells are able to mount faster and stronger attacks; occasionally, these quick-draw assaults are so powerful that the microbe is purged before it gets a second shot at infection. Other times, immune responses are too weak or sluggish to forestall infection entirely, but still strong enough to exterminate the interloper before it causes symptoms. Most people “have probably been reinfected with lots of viruses in their lives and not known it, because they didn’t get sick,” Barker told me.

Repeat tussles with the same pathogen can also come with perks. Immune cells glean more intel on invaders each time they meet them, and strengthen their skills for future bouts. That’s textbook immunology: a body learning from experience.

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.

“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.”

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.)

The coronavirus is very likely here to stay, even after the pandemic officially ends. The virus will continue to have opportunities to evolve; in its myriad forms, it will cross paths with many of us again and again. “Reinfections are probably something we’re going to have to get used to,” Barker said. But virus and human will grow accustomed to each other, reaching something of a détente; immunity will, over time, build like a seawall.

Actualizing that reality will require vigilance on our behalf, too. If repeat infections tell us anything, it’s that the less the virus mutates, the longer we’ll be able to protect ourselves against it. Viruses can’t replicate and evolve when they’re starved of hosts, and we’ve long known how to best cut the conduits they travel. To ensure our future, we might be wise to learn from our past. Perhaps our immune systems—and the virus—can relate.