McNaughton A., Paton R., Edmans M., Youngs J., Wellens J., Phalora P., Fyfe A., Belij-Rammerstorfer S., Bolton J., Ball J., Carnell G., Dejnirattisai W., Dold C., Eyre D., Hopkins P., Howarth A., Kooblall K., Klim H., Leaver S., Lee L., López-Camacho C., Lumley S., Macallan D., Mentzer A., Provine N., Ratcliff J., Slon-Compos J., Skelly D., Stolle L., Supasa P., Temperton N., Walker C., Wang B., Wyncoll D., Simmonds P., Lambe T., Baillie K., Semple M., Openshaw PIM., Obolski U., Turner M., Carroll M., Mongkolsapaya J., Screaton G., Kennedy S., Jarvis L., Barnes E., Dunachie S., Lourenço J., Matthews P., Bicanic T., Klenerman P., Gupta S., Thompson C., OPTIC consortium None., SNBTS consortium None., ISARIC4C Investigators None.

Summary It is unclear whether prior endemic coronavirus infections affect COVID-19 severity. Here, we show that in cases of fatal COVID-19, antibody responses to the SARS-COV-2 spike are directed against epitopes shared with endemic beta-coronaviruses in the S2 subunit of the SARS-CoV-2 spike protein. This immune response is associated with the compromised production of a de novo SARS-CoV-2 spike response among individuals with fatal COVID-19 outcomes.

Fatal COVID-19 outcomes are associated with an antibody response targeting epitopes shared with endemic coronaviruses

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