Key result
Post-transcriptional RNA degradation pathways, including nonsense-mediated decay and the RNA exosome, play crucial roles in restricting viral infections and preventing aberrant autoimmune responses.
This review highlights the dual role of RNA degradation pathways in restricting viral infections and preventing autoimmune diseases driven by type I interferons.
May guide RNA-targeted antivirals and immunomodulators; leaves open prospective clinical validation.
Post-transcriptional control determines the fate of cellular RNA molecules. Nonsense-mediated decay (NMD) provides quality control of mRNA, targeting faulty cellular transcripts for degradation by multiple nucleases including the RNA exosome. Recent findings have revealed a role for NMD in targeting viral RNA molecules, thereby restricting virus infection. Interestingly, NMD is also linked to immune responses at another level: mutations affecting the NMD or RNA exosome machineries cause chronic activation of defence programmes, resulting in autoimmune phenotypes. Here we place these observations in the context of other links between innate antiviral immunity and type I interferon mediated disease and examine two models: one in which expression or function of pathogen sensors is perturbed and one wherein host-derived RNA molecules with a propensity to activate such sensors accumulate.
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Rigby et al. (2015) conducted a review in Antiviral immunity and autoimmunity (e.g., type I interferonopathies). RNA degradation pathways (NMD and RNA exosome) was evaluated. Post-transcriptional RNA degradation pathways, including nonsense-mediated decay and the RNA exosome, play crucial roles in restricting viral infections and preventing aberrant autoimmune responses.
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