Type I interferons (IFNs) have broad antiviral activities through the induction of IFN-stimulated genes (ISGs). This is considered to constitute the first line of antiviral defense, but excessive exposure to IFNs provokes tissue damage and other pathological events. However, in addition to type I IFNs, the body has other innate antiviral defenses, which were commandingly reviewed by Dr Paludan in a recent issue of Trends in Immunology [1]. The article highlighted that type I IFN-independent antiviral mechanisms, including alternative antiviral cytokines (e.g., IFN-λ or interleukin 22), or the basal expression of particular ISGs, can mediate early antiviral defenses without evoking the inflammatory damage associated with the production of type I IFNs.
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