title: Molecular epidemiology of hepatitis C genotype 6a from patients with chronic hepatitis C from Hong Kong.
abstract: There have been relatively few studies on HCV genotype 6 compared to hepatitis C virus (HCV) genotype 1. In Hong Kong, a city of about 7 million people, most patients infected with HCV are infected with either genotype 1b or 6a. It is known that HCV 6 is of intermediate responsiveness (i.e., between that of HCV genotype 1 and HCV genotypes 2/3) to standard combination interferon/ribavirin therapy. This study examines the molecular epidemiology of chronic HCV 6a infection in Hong Kong during 1999-2005, as well as characterizing some pre- and post-treatment changes in the NS5B gene in a few patients that underwent combination treatment. Partial non-structural protein sequences (NS5B, the viral RNA-dependent RNA polymerase gene, positions 397-1,082) were cloned and sequenced in samples from 51 patients that were obtained and archived during 1999-2005. There were three patients with paired pre- and post-treatment samples available for further analysis. Within this NS5B sequence, one significant amino acid mutation was found in each of these patients: Ser272Pro (end-of-treatment response but relapsed), Met312Thr (failed treatment after 3 months due to anemia), and Arg221Lys (end-of-treatment-response but relapsed). This analysis of the pre- and post-treatment NS5B sequences, suggests that whilst post-treatment mutations were identifiable in individual patients, there was no overall characteristic mutation pattern associated with treatment that was common to all treated patients, identified in this small study. Larger studies are required to confirm these findings.
authors.affiliation: Department of Microbiology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong SAR, China.
authors.forename: Cheryl S Y
authors.initials: CS
authors.lastname: Li
authors.forename: Paul K S
authors.initials: PK
authors.lastname: Chan
authors.forename: Julian W
authors.initials: JW
authors.lastname: Tang
mesh_terms: D000998:Antiviral Agents / Q000494:pharmacology / Q000627:therapeutic use; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics* / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000453:epidemiology* / Q000821:virology; D006723:Hong Kong / Q000453:epidemiology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology / Q000627:therapeutic use; D017720:Molecular Epidemiology; D008969:Molecular Sequence Data; D009154:Mutation; D010802:Phylogeny; D011092:Polyethylene Glycols; D011994:Recombinant Proteins; D012254:Ribavirin / Q000494:pharmacology / Q000627:therapeutic use; D017422:Sequence Analysis, DNA; D016896:Treatment Outcome; D017361:Viral Nonstructural Proteins / Q000737:chemistry / Q000187:drug effects / Q000235:genetics; D012324:RNA-Dependent RNA Polymerase
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011092:Polyethylene Glycols; D011994:Recombinant Proteins; D012254:Ribavirin; D017361:Viral Nonstructural Proteins; C087036:NS-5 protein, hepatitis C virus; D012324:RNA-Dependent RNA Polymerase; C417083:peginterferon alfa-2b