IFNAR1 and viral infectious disease: These results indicate that, the IFN-I response generally elicited during all viral infection induces CSR to IgG2c of some antigen-specific B cells, and this effect is unlikely limited to LCMV infection or more broadly, persistent infections; thus, neither the diminished NP-specific IgG1 Ab response observed during LCMV infection nor its recovery upon IFNAR blockade is accounted for by a skewing toward or away from IgG2c responses.