Such responses include secretory IgA, mucosal-homing plasmablasts, and resident memory T cells.8, 9, 10 As compared to IgG, the polymeric structure of secreted IgA molecules may contribute to superior virus neutralization potency, and possibly greater breadth of neutralization of antigenically-diverse viruses.11, 12, 13 In mouse models of influenza, passive administration of purified IgA to the respiratory tract can protect against infection, and (unlike serum IgG) appears capable of abrogating nasal virus shedding at levels matching those seen in previously-infected convalescent animals.12 This evidence concerns the gene CD79A and infection.