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Adam Kucharski, MMath, PhD

There are now several studies that, taken together, give us a useful indication of the possible role of preexisting immunity (antibodies/T cells, etc.) in SARS-CoV-2 dynamics.

Here are my thoughts, plus some helpful links, on the matter.

First, there are several well-defined outbreaks in which a very large percentage of people had detectable infection (either a positive PCR or detectable antibody levels). There were 103 cases out of 117 people on a fishing boat, 11 out of 13 individuals who attended the same meeting, and 7 out of 8 and then 8 out of 8 of those who ate a meal together.

This would suggest that there is not a substantial percentage of the adult population that cannot get infected if exposed to this novel coronavirus. This conclusion is consistent with other data from healthcare workers and care homes.

If there is enough exposure and you look hard enough, it seems you will find infections.

But just because the majority of people are vulnerable to infection does not mean that there is no immunity at all. In a study of individuals during the previously mentioned outbreak on the fishing boat, a small number (3 out of 120) had neutralizing antibodies, perhaps from earlier SARS-CoV-2 infection. They did not get infected again.

Then there's children. There is evidence that they may be less susceptible to infection. Some younger kids not previously exposed to SARS-CoV-2 also have cross-reactive antibodies, which may help explain the reduced risk.

So far we've been talking about immunity against infection. However, there is also the question of protection against disease. Clearly some people get less severe symptoms, suggesting some role of disease immunity.

There's evidence of some pre-existing T-cell responses in individuals who have not been infected with SARS-CoV-2. For people who have been infected with SARS-CoV-2, T-cell responses can persist after infection.

This would be good news, and consistent with circulating seasonal "common cold" coronaviruses, which can reinfect people but seem to result in milder symptoms on reinfection.

It's important to note that protection from infection affects epidemic dynamics more than protection from disease. In herd immunity calculations, what matters is whether people transmit, not how ill they get (although the two may be correlated). So immunity against disease won't necessarily stop outbreaks.

It's also worth remembering that any preexisting immunity from infection (eg, among children) is already "priced into" the reproduction number; the rapid growth early in the pandemic would have been in spite of any preexisting immunity. So we need to be careful about interpreting how immunity might influence dynamics.

Obviously there's still a lot more we need to learn about SARS-CoV-2 immunity. I will be interested to hear about any other emerging studies that shed light on this issue (or whether immunologists want to flag anything I've missed).

For those of you particularly interested in this issue, I would recommend a useful primer published in The Atlantic written by Ed Yong, a science writer, about why these immunology questions are important and very challenging.

Adam Kucharski is an epidemiologist whose research focuses on the dynamics of infectious diseases, including how social behavior and immunity shape disease transmission, and how knowledge of such processes can enhance control measures. Follow him on Twitter

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COVID-19 Data Dives: Preexisting Immunity to SARS-CoV-2 Is a Thing - Medscape