Cellular antiviral responses against influenza A virus are countered at the posttranscriptional level by the viral NS1A protein via its binding to a cellular protein required for the 3' end processing of cellular pre-mRNAS.

摘要: Abstract The influenza A virus NS1 protein (NS1A protein) binds and inhibits the function of 30-kDa subunit CPSF, a cellular factor that is required for 3′-end processing pre-mRNAs. Here we generate recombinant A/Udorn/72 encodes an NS1A containing mutated binding site CPSF. This mutant substantially attenuated, indicating this in efficient replication. Using virus, show to CPSF mediates viral posttranscriptional countermeasure against initial antiviral response—the interferon-α/β (IFN-α/β)-independent activation transcription genes, which requires interferon regulatory factor-3 (IRF-3) activated by infection. Whereas these pre-mRNAs inhibited cells infected wild-type functional mRNAs are produced virus. These results establish largely responsible inhibition Mutation also affects second response: IFN-β mRNA earlier larger amounts.