Innate Antiviral Defenses Independent of Inducible IFNα/β Production

The type I interferons (IFNs) (IFNα and IFNβ) not only have potent antiviral activities, but also have pathological functions if produced at high levels or over a long time. Recent articles have described antiviral immune mechanisms that are activated in response to virus infection at epithelial surfaces independently of IFNα and IFNβ. This may allow the host to exert rapid local antiviral activity and only induce a full-blown, and potentially pathological, type I IFN response in situations where stronger protective immunity is needed. Here, I describe the emerging understanding of early antiviral defenses, which are independent of type I IFN responses, and also discuss how this enables tissues to exert rapid antiviral activities and to limit type I IFN production.

TrendsExcessive and prolonged expression of type I IFN is pathological to the organism, and uncontrolled production of type I IFNs is associated with inflammatory diseases.Epithelial surfaces have antiviral mechanisms that are activated rapidly after infection and exert type I IFN-independent antiviral activity.Defects in the ability to mount type I IFN-independent antiviral activity lead to early elevated viral loads and higher expression of type I IFNs.As the type I IFN response start to develop in the tissue, several check-points are used to ensure a gradual build-up of the response.