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The mouse genome encodes a family of Oas proteins that synthesize 2′-5′A in response to dsRNA. 2′-5′A activates the endonuclease RNase L to cleave single-stranded viral and cellular RNAs. The inactive, full-length Oas1b protein confers flavivirus-specific disease resistance. Although similar numbers of neurons were infected in resistant and susceptible brains after an intracranial virus infection, viral components amplified only in susceptible brains at later times. A line of resistant RNase L−/− mice was used to evaluate the contribution of RNase L to the resistance phenotypein vivo . Activation of RNase L antiviral activity by flavivirus infection was indicated by increased viral RNA levels in the brains of RNase L−/− mice.Oas1a andOas1b mRNA levels were higher in infected RNase L−/− mice, indicating that activated RNase L also have a proflaviviral affect. However, the resistance phenotype was equally robust in RNase L−/− and RNase L+/+ mice.

RNase L Antiviral Activity Is Not a Critical Component of the Oas1b-Mediated Flavivirus Resistance Phenotype