Immunity Primer

People who recover from an infection with SARS-CoV-2 / HCov-19 are likely to be immune for some time. That is, the virus is “immunizing”. To understand why this is likely to be the case, we need a quick primer on immunology.

When you’re infected with a virus, the first immune response you mount is an innate immune response. This is largely non-specific. It acts to limit virus replication in ways that are more or less agnostic to the type of virus. For example, it kills infected cells, preventing them from producing new virus particles (virions). Later in infection, you mount an adaptive immune response. This is a more targeted response. Your body develops antibodies that recognize proteins on a virion and bind to them. Often, these are neutralizing: they make virions non-viable. For example, many antibodies to the influenza virus bind to a protein called HA that the influenza virion uses to enter cells, thus preventing it from doing so.

After you’ve gotten rid of all the viable virus in your body (“cleared” the infection), the white blood cells that produced those antibodies don’t all go away. You keep some of them around to mount a faster and more powerful response if you’re ever reinfected. These are called memory B-cells.

Immune memory against flu is actually fairly protective, just as it is against measles or chickenpox. So why do you have to get the flu vaccine every year? Because the virus evolves in response to our immunity. Under the selection pressure imposed by antibody immunity, the influenza HA protein eventually changes, rendering old antibodies unable to bind to it as effectively. Chickenpox and measles induce longer lasting immunity because the targets of our antibodies don’t evolve as readily.

The new coronavirus takes a long time to be cleared from the body, which suggests that the innate response alone is not sufficient, and an adaptive response is required. But the fact that the vast majority of people do recover suggests that we can and do make neutralizing antibodies against the virus. So I expect recovered individuals to be immune to the virus, at least in the short term. Whether the virus will ultimately evolve to escape that immunity (like flu) or will be more like chickenpox or measles remains to be seen.

Furthermore, since I wrote the above, a medRxiv preprint has been posted. The authors experimentally infected four macqaques, and then “re-challenged” (tried to infect again) two of the three monkeys who recovered. Neither recovered monkey developed disease a second time, suggesting the presence of protective immunity. A monkey is not a human, of course, but this is more promising and suggestive evidence.

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Dylan H. Morris
PhD Candidate, Ecology & Evolutionary Biology

I’m a PhD candidate in Ecology & Evolutionary Biology interested in mathematical biology, population genetics, and virus ecology and evolution.