For SARS-CoV-2, there is growing evidence that exposure to other coronaviruses — including those that cause colds and other respiratory illnesses — plays a part in people’s immune responses. “Much like flu, most of us are infected with these common coronaviruses by the age of five or six,” says Scott Hensley, a microbiologist at the University of Pennsylvania in Philadelphia. His group discovered that blood serum samples taken from people before the pandemic contained antibodies against a common-cold coronavirus called OC43 that could bind to the SARS-Cov-2 spike protein2.

Using samples taken before and after SARS-CoV-2 infection, Hensley and his colleagues were able to show that catching SARS-CoV-2 boosted the production of OC43-binding antibodies. Their study, published in April, found that these antibodies bound to the S2 subunit of the SARS-CoV-2 spike protein — which has a similar structure to that in OC43. But the OC43 antibodies did not bind to the S1 region of the SARS-CoV-2 spike and were unable to stop the virus entering cells.