Key result
This review discusses the mechanisms by which cytosolic RNA helicases detect viral double-stranded RNA to induce antiviral immunity through RNA interference and interferon signaling pathways.
This review summarizes the mechanisms by which cytosolic RNA helicases detect viral double-stranded RNA to induce antiviral immunity via RNA interference and interferon signaling.
Informs species-specific antiviral signaling; leaves open clinical translation to viral myocarditis or cardiomyopathy.
A key aspect of antiviral immunity is the distinction between "self" and "non-self" components. This distinction can be established through the detection of double-stranded RNA (dsRNA), a common sign of viral infection, by cytosolic RNA helicases. Depending on the organism, two major antiviral pathways can be induced by dsRNA helicases: RNA interference (RNAi) and interferon (IFN) signaling. In the RNAi pathway, dsRNAs are recognized by a Dicer protein, and are then used for the sequence-dependent recognition and subsequent degradation of the complementary viral RNAs. In the IFN signaling pathway, dsRNAs are recognized by a RIG-like receptor (RLR), which induces a signaling cascade in order to induce the expression of IFNs, cytokines and chemokines. In this review, we discuss the RNA features that can be used by the cell to detect a viral infection, the two aforementioned types of helicase-mediated sensing, as well as some viral escape mechanisms developed to avoid recognition.
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Rousseau et al. (2020) conducted a review in Viral infection. This review discusses the mechanisms by which cytosolic RNA helicases detect viral double-stranded RNA to induce antiviral immunity through RNA interference and interferon signaling pathways.
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