title: Targeting hepatitis C virus translation: stopping HCV where it starts.
abstract: Hepatitis C virus (HCV) infection is an emerging global health concern. Combination therapy with pegylated interferon-alpha (INF alpha) and ribavirin results in approximately 60% sustained recovery. Of the non-responders, the majority are infected with genotype 1. As a consequence, improved therapeutics are necessary to enhance response rates, especially in genotype-1-infected individuals. HCV translation is mediated by an internal ribosome entry site (IRES) located within the 5' non-translated region. Recent studies have revealed that the HCV IRES recruits the cellular translation machinery in a distinct manner compared with cellular mRNA strategies. Therefore, screening assays can be developed to identify specific inhibitors of HCV translation as a possible treatment for HCV.
authors.affiliation: Schering-Plough Research Institute, Department of Antiviral Therapy, 2015 Galloping Hill Road, Mailstop 4945, Kenilworth, NJ 07033, USA. ronald.jubin@spcorp.com
authors.forename: Ronald
authors.initials: R
authors.lastname: Jubin
mesh_terms: D000818:Animals; D004353:Drug Evaluation, Preclinical; D016174:Hepacivirus / Q000187:drug effects* / Q000235:genetics*; D006526:Hepatitis C / Q000517:prevention & control*; D006801:Humans; D014176:Protein Biosynthesis / Q000187:drug effects*; D011817:Rabbits; D012156:Reticulocytes / Q000187:drug effects; D012270:Ribosomes / Q000187:drug effects / Q000821:virology