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-methylguanine 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.

Keywords:
cap, 7-methyl-guanine nucleotide, elF, eukaryotic initiation factor, EM, electron microscopy, HCV, hepatitis C virus, IRES, internal ribosome-entry site, UTR, untranslated region, elF3, HCV, IRES, translation
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© 2002 Biochemical Society
2002
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