As such, we expected that supplemental IFN-I stimulation with poly I:C post-CB4 infection would abrogate the IFN-I signature with higher systemic IFN-I levels and polarized T cell responses typically observed in CB4-infected, untreated MDA5+/- mice would shift to effector rather than regulatory CD4+ T cells dominating in the PLNs. This evidence concerns the gene CD4 and infection.