Double‐stranded RNA interference (dsRNAi) represents a primary means of anti‐viral defense in plants, worms, and insects, yet appears mostly supplanted by the protein‐based interferon (IFN) response in vertebrates such as mammals. The degree to which dsRNAi is anti‐viral in mammals has been contentious. Maillard et al (2016) find that dsRNAi retains sequence‐specific silencing in mammalian cells incapable of triggering an IFN response, suggesting that dsRNAi is inhibited by the action of interferon‐stimulated genes. Importantly, they observe that while dsRNA can “vaccinate” against the incoming cognate virus though dsRNAi silencing, no dsRNAi is observed with viral infection alone, suggesting that this evolutionarily conserved anti‐viral pathway is present but functionally elusive in the cell types studied thus far.
See also: PV Maillard et al
RNA interference (RNAi) is a mechanism conserved in most eukaryotes that enables sequence‐specific gene silencing via the use of small RNAs 22–30 nt in length. As an anti‐viral defense system, RNAi operates by sensing and fragmenting viral dsRNA through the action a Dicer RNase. The resulting small interfering RNAs (siRNAs) then guide Argonaute (Ago) effector proteins in an RNA‐induced silencing complex (RISC) to cleave target RNA sequences bearing siRNA complementarity. This core system to sense and process dsRNA via Dicer into siRNAs that guide Agos is the hallmark of dsRNAi and is distinct but related to the role of these proteins in gene regulation via microRNAs (miRNAs) (tenOever, 2016). In plants and invertebrates, dsRNAi plays a critical role in suppressing viral accumulation and provides a systemic immune response (tenOever, 2016 …
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