IFNA1 and viral infectious disease: To confirm that optineurin protein synthesis was directly activated by virus infection and not indirectly through a response to IFN, we repeated the SeV infections in cells engineered to constitutively express a functional V protein of Parainfluenza virus-5 (PIV5) that blocks IFN signaling (Hep2/PIV5-V cells) (Figure S1A) [27],[28] and in Vero cells, which lack the genes for type I interferon [29].