The current study offers a mechanistic explanation for these live infection data: (1) live infection produces virions; (2) the consensus features of virion structures, i.e., ED and iNA in the context of a virion-sized structure, can robustly activate naïve Ag-specific B cells to initiate class-switch recombination and secrete IgG that is independent of viral replication or any other adjuvants; and (3) the IgG has an intrinsically slow off-rate that can offer an effective neutralization of cognate virions. This evidence concerns the gene RENBP and infection.