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Significance The OAS–RNase L system is an innate immunity pathway activated by viral infection. Viral dsRNA stimulates OAS enzymes to produce short 2′,5′-oligoadenylates (2-5A) that activate RNase L, resulting in cleavage of single-stranded (ss) RNA. We discovered a small-molecule inhibitor of RNase L that rescues the toxic phenotype of cells deficient in the dsRNA-editing enzyme ADAR1. ADAR1 destabilizes dsRNA to prevent OAS activity.ADAR1 mutations are responsible for a subset of cases of Aicardi-Goutières syndrome (AGS), a severe neurodevelopmental and inflammatory genetic disease of children with no effective medical therapy. We posit that an RNase L inhibitor may have utility against cases of AGS in which RNase L is activated and other indications where overactivation of RNase L is harmful.

A phenolic small molecule inhibitor of RNase L prevents cell death from ADAR1 deficiency