Cell https://doi.org/10.1016/j.cell.2020.11.029 (2020)

Since the recent onset of the COVID-19 pandemic, there have been some reports of suspected cases of reinfection by SARS-CoV-2. The question remains, however, of whether SARS-CoV-2 viral infection can elicit durable immunologic memory responses or whether memory generation is somehow impeded by viral virulence mechanisms. In Cell, Rodda et al. report a longitudinal analysis of adaptive immune memory that had arisen in patients who had experienced mild COVID-19 disease and had recovered. Blood samples taken at 1 and 3 months post-symptom onset contain circulating antibodies specific for the receptor-binding domain (RBD) of the SARS-CoV-2 spike (S) protein, which are capable of inhibiting the interaction with the host ACE2 viral receptor, suggesting that long-lived plasma cells had been generated. RBD-specific memory B cells, identified by tetramer enrichment, are present in convalescent blood and increased in frequency at the later time point. Monoclonal antibodies generated from a subset of these memory B cells are capable of blocking the RBD–ACE2 interaction and neutralizing the virus. Likewise, at 3 months post-infection, patients who have recovered harbor S-specific memory CD8+ and CD4+ T cells, including circulating CXCR5+ follicular helper T cells and CXCR3+ central memory T cells, that respond to restimulation by proliferating and producing cytokines. Thus, durable adaptive memory can arise in response to community-acquired SARS-CoV-2 infection and can potentially provide protection to secondary exposure.