IFNA1 and viral infectious disease: Overexpression of MCCC1 potentiated virus-triggered activation of the IFN and pro-inflammatory cytokine promoters and induction of the endogenous IFN and pro-inflammatory cytokine genes, whereas MCCC1 knockdown had the opposite effect, suggesting that MCCC1 is an important component of innate immune signaling pathways in response to viral infection.