Conformational inhibition of the hepatitis C virus internal ribosome entry site RNA.

ABSTRACT: The internal ribosome entry site (IRES), a highly conserved structured element of the hepatitis C virus (HCV) genomic RNA, is an attractive target for antiviral drugs. Here we show that benzimidazole inhibitors of the HCV replicon act by conformational induction of a widened interhelical angle in the IRES subdomain IIa, which facilitates the undocking of subdomain IIb from the ribosome and ultimately leads to inhibition of IRES-driven translation in HCV-infected cells.

SUBMITTER: Parsons J 

PROVIDER: S-EPMC2770845 | biostudies-literature | 2009 Nov

REPOSITORIES: biostudies-literature