Can You Get COVID-19 More Than Once?

Evidence is mounting that the answer is yes—but no one knows how often this could happen.

covid-19 PCR test

Medically reviewed in October 2020

Updated on November 3, 2020

News of the first person in North America known to have been reinfected by SARS-CoV-2 recently made headlines and dimmed hopes for herd immunity—which occurs when enough people are immune to a disease by either getting infected or being vaccinated, making the spread of this disease from person to person unlikely.

This report of a previously healthy 25-year-old Nevada man twice sickened by COVID-19 is the fifth reinfection case to be described in medical research. There have also been reports that antibodies to the coronavirus can vanish or dwindle over time.

Now, fears are rising that herd immunity (also called herd protection) to COVID-19 may not be readily achievable.

Are COVID-19 survivors really at risk of getting it again?

Evidence is growing that reinfection is possible. But we still don’t know how common, likely or significant reinfection may be. The immune system’s interaction with this coronavirus, which was identified only about ten months ago, remains a new field of study.

Scientists suspected early on that people who recover from COVID-19 could be reinfected. That’s the case with most betacoronaviruses, a subtype that includes SARS-CoV-2, according to David Sullivan, MD, a professor of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland.

“From the very beginning, in March, most people were predicting you could get reinfected, as per most betacoronaviruses,” says Dr. Sullivan. “It’s not going to surprise us if people can get it a year later.”

Still, the fact that only five cases of reinfection have been reported worldwide so far could suggest that reinfection is rare. Or perhaps it only rarely comes to researchers’ attention. Surveillance for SARS-CoV-2 remains spotty, so reinfection could be common. We just don’t know yet.

“We are probably severely underestimating the number of asymptomatic reinfections,” wrote Yale immunologist Akiko Iwasaki, PhD, in an editorial published on October 12 in The Lancet along with the report of the Nevada man.

In the case of the Nevada man, the evidence of genuine reinfection was strong. Researchers demonstrated that the viral strain isolated after his second positive test differed genetically from the one he had at first. This suggests he had true separate encounters with separate strains, both of which made him sick. He also tested negative between the two confirmed infections.

But less clear-cut cases of potential reinfection could be due to a long course of infection, inaccurate tests or the possibility that the coronavirus could hide out in the body, then reemerge later.

Indeed, in a May 2020 Korean study of people testing positive twice, researchers were unable to grow live virus out of the “re-positive” samples. Nor could they demonstrate that people testing positive for a second time had infected anyone else.

The role of antibodies
Once the immune system “sees” coronavirus, it takes 1 to 2 weeks for antibodies to form. These proteins recognize virus in bodily fluids, stick to it, and, in some cases, render it harmless, ready to be cleared away by other parts of the immune ystem.

Over time, antibody levels can fall. One small August 2020 study published in Nature Medicine involving people infected with SARS-CoV-2 without symptoms found that many had undetectable antibody levels three months later. Research also suggests that the number of neutralizing antibodies—the most protective kind—dwindles a few weeks after symptoms begin.

But here’s some good news: The body has other ways of defending itself.

T-cells and B-cells also matter
Unlike the innate immune system, which launches a general attack to invading pathogens, the body also has an adaptive, or acquired immune system, which responds to exposure to a specific pathogen.

This adaptive arm, which kicks into action when the innate immune system alone isn’t able to control an infection, includes two types of cells that learn from experience: T-cells and B-cells. Both of these immune cells play important roles in the body’s response to pathogens like SARS-CoV-2.

B-cells are antibody factories, while T-cells support B-cells and kill virus-infected cells outright.

Antibody levels may fall after infection. But T-cells and B-cells that the immune system deployed to fight off the infection (or that a vaccine has taught the body to make) can be stored by the immune system for years, where they remain ready to do battle if the virus ever returns.

There’s already evidence that the body forms strong T-cell responses to SARS-CoV-2. Some people even do this without an antibody response, leading some researchers to predict that measuring T-cells may prove better than measuring antibodies to check for immunity. (Antibody testing used in screening the public is prone to false positives, anyway, in part because positive results could reflect antibodies to some other coronaviruses.)

This protection can be long-lasting. Survivors of the 2003 SARS epidemic were recently reported to retain protective memory T-cells up to 17 years later.

Moreover, some people who have never been infected with SARS-CoV-2 still carry T-cells that react to it. These most likely formed against viruses that cause the common cold. They were similar enough to recognize, at least to some degree, the more serious new coronavirus.

Still, Sullivan warns, we don’t know yet how long SARS-CoV-2-specific memory immune cells might last. “Is it a short-term memory or a long-term memory? We don’t really have enough evidence yet to characterize that,” he says, noting that “we’re successfully one-and-done for many viruses, but not for influenza.”

Other lines of defense
Some research suggests that if reinfection does occur, it may be mild. An August 2020 study of macaque monkeys infected with SARS-CoV-2 published in Science found them immune to a second bout, at least if they encountered it during early recovery. In studies of other types of coronavirus infection in both animals and people, milder infections led to short-lived immunity. Severe ones, meanwhile, including those caused by SARS and MERS, may be associated with longer-lasting protection.

But in two of the world’s five reports of reinfection, people experienced worse symptoms the second time around. The Nevada man was one. He weathered his first bout at home, but the second time, he was hospitalized and required oxygen. It’s unknown whether that was because the second viral strain was more virulent, if he got a high dose of virus the second time or because his immune system reacted to reinfection in a way that led to worse disease.

While scientists continue to investigate and learn more about how SARS-CoV-2 affects the body, vaccines are on the way.

In a July 31, 2020 editorial published by The New York Times, Iwasaki and her fellow Yale immunologist Ruslan Medzhitov, PhD, stated unequivocally that falling antibody counts don’t diminish the odds that we’ll develop a useful vaccine. The scientists have noted that one main advantage of vaccines over the body’s natural immune response is that they can be designed to target virus’ weaknesses.

And we shouldn’t necessarily worry that the Nevada case implies that we’ll need separate vaccines for each strain. As Iwasaki wrote in his October editorial, one vaccine should suffice against all the strains in circulation.

She warned, however, that reinfection cases mean we can’t count on whatever immunity we gain from infection to give us herd immunity. We will need vaccines.

Adjuvants, which are ingredients used in some vaccines, can also be used to bolster the body’s immune response, the Centers for Disease Control and Prevention explains.

Sullivan and his colleagues at Johns Hopkins University are also conducting randomized controlled trials, which are investigating the use of antibody-rich convalescent plasma to treat people with COVID-19. The treatment involves the introduction of antibodies from another person who has recovered from the disease to achieve what’s known as “passive immunity.”

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