The hepatitis C virus internal ribosome-entry site: a new target for antiviral research.
The hepatitis C virus (HCV) is the main causative agent of non-A, non-B hepatitis in humans and a major cause of mortality and morbidity in the world. Currently there is no effective treatment available for the infection caused by this virus, whose replication depends on an unusual translation-initiation mechanism. The viral RNA contains an internal ribosome-entry site (IRES) that is recognized specifically by the small ribosomal subunit and by eukaryotic initiation factor 3, and these interactions allow cap (7-methyl-guanine nucleotide)-independent initiation of viral protein synthesis. In this article, we review the structure and mechanism of translation initiation of the HCV IRES, and its potential as a target for novel antivirals.
Gallego
J
J
MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, U.K. jgs@mrc-lmb.cam.ac.uk
Varani
G
G
D000998:Antiviral Agents / Q000494:pharmacology*; D001483:Base Sequence; D016174:Hepacivirus / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism* / Q000472:pathogenicity; D006801:Humans; D008969:Molecular Sequence Data; D009690:Nucleic Acid Conformation; D010442:Peptide Chain Initiation, Translational; D012367:RNA, Viral / Q000737:chemistry / Q000235:genetics; D012270:Ribosomes / Q000187:drug effects / Q000378:metabolism*
D000998:Antiviral Agents; D012367:RNA, Viral