Upon viral infection, mammalian hosts launch an immediate innate immune response, including the production of IFNs, particular type I IFN (IFN-α/β) and type III IFN-lambda (IFN-L), which further bind to their corresponding surface heterodimeric receptors (IFNAR for type I IFN; IFNLR1 and IL10RB for IFN-L), leading to the activation of the Janus kinase 1 (JAK1)-signal transducer and activator of transcription 1/2 (STAT1/2) pathways, thus subsequently leading to a variety of ISGs expression to control invading viruses (14, 25, 26, 30, 54). This evidence concerns the gene IFNA1 and viral infectious disease.