Last updated: 31 March 2020. First published: 31 March 2020
Why immunity matters
Among the most important questions about COVID-19 is whether those who recover from infection gain immunity, and for how long.
Immunity is common. It’s why most people only get chicken pox once in their lives; and why vaccinations against diseases like measles, mumps, rubella, and (back in the day) polio work. We take (or should take) an annual flu vaccine, which gives us significant protection against that year’s strain, which puts pressure on the influenza virus to mutate in order to evade those defenses next year.
There are at least four reasons why it’s critical to know more about acquired COVID-19 immunity.
First, the most plausible way that the epidemic will end is via herd immunity: when enough people in a given population have recovered and gained immunity, the virus has fewer people left to infect, and the effective reproductive number drops below one. Without acquired immunity for a reasonable amount of time, the virus could continue circulating and reinfecting us for an indefinite amount of time.
Secondly, if there is acquired immunity, recovered people can serve safely on the front lines; otherwise, we could run out of health care providers. And recovered people can also return to work safely, allowing us to restart the economy.
Finally, any prospect of a vaccine depends on acquired immunity.
What do we currently know?
The vast majority of experts I’ve read or spoken to believe that we will acquire at least temporary immunity; but we still don’t know for certain.
There are many reasons to expect that we will:
- Patients recover from COVID-19 because their immune system rallies against the virus. With many viruses, this means that the immune system creates antibodies that defend against that specific virus; and in many cases, this immunity persists.
- Such antibodies seem to be appearing in recovered patients. (Here’s a second paper on the topic.)
- Macaques seem to gain neutralizing antibodies and resist further infection.
- With past coronaviruses, individuals gained at least temporary immunity.
But we should also be cautious.
- There are some reports of re-infection, though most scientists believe that these patients had not in fact fully recovered.
- RNA viruses like COVID-19 mutate easily. In the case of influenza, it successfully mutates every year to evade our prior defenses.
Here are the best, relatively recent articles I’ve found, with key excerpts.
The answer is a qualified yes, with some significant unknowns.
A study in macaques infected with the new coronavirus suggested that once infected, the monkeys produce neutralizing antibodies and resist further infection.
Most people who became infected during the SARS epidemic — that virus is a close cousin of the new coronavirus, called SARS-CoV-2 — had long-term immunity lasting eight to 10 years
Those who recovered from MERS, another coronavirus, saw much shorter-term protection
Though COVID-19 likely makes recovered patients immune, experts aren’t sure how long protection lasts
One brush with the viruses that cause chickenpox or polio, for instance, is usually enough to protect a person for life. Other microbes, however, leave less of an impression, and researchers still aren’t entirely sure why. This applies to the four coronaviruses known to cause a subset of common cold cases, says Rachel Graham, an epidemiologist and coronavirus expert at the University of North Carolina at Chapel Hill. Immunity against these viruses seems to wane in a matter of months or a couple of years, which is why people get colds so frequently.
Reports have surfaced in recent weeks of people who have tested positive for the virus after apparently recovering from COVID-19, fueling some suspicion that their first exposure wasn’t enough to protect them from a second bout of disease. Most experts don’t think these test results represent reinfections. Rather, the virus may have never left the patients’ bodies, temporarily dipping below detectable levels and allowing symptoms to abate before surging upward again. Tests are also imperfect, and can incorrectly indicate the virus’ presence or absence at different points.
The authors chalked the protection up to the antibodies they found in the monkeys’ bodies, apparently produced in response to the virus—a result that appears to echo the detection of comparable molecules in human COVID-19 patients.
But the mere presence of antibodies doesn’t guarantee protection, Wang says. Reinfections with common cold coronaviruses can still happen in patients who carry antibodies against them. And a bevy of other factors, including a person’s age and genetics, can drastically alter the course of an immune response.
Occasionally, however, mutations will alter a viral strain so substantially that the immune system can no longer recognize it, sparking an outbreak—even in populations that have seen a previous version of the virus before.
So far, SARS-CoV-2 also doesn’t appear to be undergoing any extreme mutations as it sweeps across the globe. That may be because it’s already hit on such a successful strategy, and doesn’t yet need to change its tactic. “Right now, it’s seeing a completely naive population” that’s never been exposed to the virus before, Graham says. The virus “doesn’t seem to be responding to any kind of pressure,” she adds.