Systemic bacterial or viral infections in vivo typically establish a Th1-polarizing environment whereby additional cytokines such as IL-12 induce expression of the Th1-lineage-defining transcription factor (TF) T-bet, and T-bet target genes such as Ifng (IFN-γ), which reinforce Th1 status (6–8). Here, IFNG is linked to viral infectious disease.