Abstract
Virus infection activates RNase L, an interferon (IFN)-regulated endoribonuclease, to cleave viral and cellular RNAs. The RNase L-cleaved, double-stranded RNA products induce formation of antiviral stress granules (avSGs) and recruit antiviral proteins RIG-I, PKR, OAS, and RNase L to avSG to amplify IFN production. Manivannan et al. (e00205-20) identified a novel role of avSGs induced by RNase L as an antiviral signaling hub to coordinate RNA ligands with cognate receptors to mount an effective host response during viral infection. These findings shed light on the importance of asSGs for host immunity.
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