Because of its OAS-like qualities (activation by IFN and binding to dsRNA) and inactive nucleotidyltransferase domain, OASL has been assumed to interfere with the 2-5A and RNase L pathway by competing with OAS.29, 30 An SNP study of the response to IFN therapy for chronic hepatitis C suggested that OASL might negatively regulate the antiviral function of OAS. This evidence concerns the gene IFNA1 and chronic hepatitis C virus infection.