Fig. 1. B cell response to SARS-CoV-2 infection.

a | Severe infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces a robust extrafollicular response but an impaired germinal centre (GC) B cell response in some individuals. Antigen-engaged B cells differentiate into memory B cells and short-lived plasmablasts that give rise to antibodies with a low level of somatic hypermutation. b | Mild SARS-CoV-2 infection induces both an extrafollicular response and GC B cell response. The GC B cell response gives rise to affinity-matured memory B cells and long-lived plasma cells. c | There is an increase in the number of SARS-CoV-2-specific memory B cells over time following mild infection. Memory B cells derived from the GC undergo continued clonal evolution for at least 1 year, with memory B cells found at later time points displaying increased levels of somatic hypermutation and encoding antibodies with enhanced neutralizing activity and breadth. The SARS-CoV-2-specific antibody titre decreases over the first 6 months following infection owing to the loss of antibodies derived from short-lived plasmablasts. The loss in protection attributable to this decrease in antibody titre is partially offset by a per antibody increase in neutralizing titre and breadth, likely owing the emergence of clonally evolved plasma cells from the GC. T_FH cell, T follicular helper cell.