title: Future trends in managing hepatitis C.
abstract: Despite recent improvements in the treatment of patients who have chronic hepatitis C, a large proportion of patients do not achieve viral clearance. Treatment regimens are also costly, associated with significant morbidity, require substantial patient commitment, and are not appropriate for all patients. Therefore, it is important to maximize and enhance current therapeutic approaches and to investigate new approaches and therapies. Because the ability to maintain adherence to current treatment is associated with higher sustained virologic response rates (particularly in patients infected with genotype 1), strategies directed at patients and support staff to promote treatment adherence are important. Other strategies to enhance current therapy include alternative interferons (IFNs)/cytokines and new IFN delivery systems. Current therapy may also be enhanced by new ribavirin (RBV) analogs with an improved safety profile or by the addition of other immunomodulatory agents such as inosine 5'-monophosphate dehydrogenase inhibitors, histamine dihydrochloride, thymosin alfa 1, and amantadine. Some of these agents have demonstrated promising results, although further evaluation is required. Greater knowledge of the molecular biology of the hepatitis C virus (HCV) holds promise for the development of targeted therapies such as specific inhibitors of HCV polymerase, protease, or helicase, as well as therapeutic vaccines. Other potential molecular-based therapies include antisense oligonucleotides, ribozymes, and short interfering ribonucleic acid (RNA) molecules. Therapies aimed at reducing or preventing the development of fibrosis are also under investigation. Multiple-drug regimens will likely be required to enhance viral clearance and reduce viral resistance, while providing greater tolerability.
authors.affiliation: Division of Gastroenterology and GI/Hepatology Research, Duke Clinical Research Institute, Duke University Medical Center, P.O. Box 17969, Durham, NC 27710, USA. mchut001@mc.duke.edu
authors.forename: John G
authors.initials: JG
authors.lastname: McHutchison
authors.forename: Anouk T
authors.initials: AT
authors.lastname: Dev
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005544:Forecasting; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000628:therapy* / Q000821:virology; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D016376:Oligonucleotides, Antisense / Q000235:genetics / Q000627:therapeutic use; D011092:Polyethylene Glycols / Q000627:therapeutic use; D016337:RNA, Catalytic / Q000235:genetics / Q000627:therapeutic use; D011994:Recombinant Proteins; D012254:Ribavirin / Q000819:agonists / Q000627:therapeutic use; D014612:Vaccines / Q000627:therapeutic use
chemical_list: D000998:Antiviral Agents; D004791:Enzyme Inhibitors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D016376:Oligonucleotides, Antisense; D016337:RNA, Catalytic; D011994:Recombinant Proteins; D014612:Vaccines; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a