Antibody Responses to SARS-CoV-2: Let's Stick to Known Knowns

Abstract

The scale of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has thrust immunology into the public spotlight in unprecedented ways. In this article, which is part opinion piece and part review, we argue that the normal cadence by which we discuss science with our colleagues failed to properly convey likelihoods of the immune response to SARS-CoV-2 to the public and the media. As a result, biologically implausible outcomes were given equal weight as the principles set by decades of viral immunology. Unsurprisingly, questionable results and alarmist news media articles have filled the void. We suggest an emphasis on setting expectations based on prior findings while avoiding the overused approach of assuming nothing. After reviewing Ab-mediated immunity after coronavirus and other acute viral infections, we posit that, with few exceptions, the development of protective humoral immunity of more than a year is the norm. Immunity to SARS-CoV-2 is likely to follow the same pattern.

Figure 1:. Kinetics of primary and secondary antibody responses against acute viral infections.

Early in the primary response, antibodies are contributed exclusively by extrafollicular plasmablasts and plasma cells (blue line). As the response progresses, germinal center-derived (green line) plasma cells with longer lifespans emerge and gradually increase in contribution to total antibody levels (purple line). Booster immunizations or re-infections trigger a memory B cell response, leading to a rapid rise in antibody levels through both germinal center-independent and -dependent mechanisms, and are often followed by a rapid decrease to levels just above pre-challenge concentrations.