title: Mode of HCV infection examined by polymorphism of hypervariable region-1 in cases of acute hepatitis C after accidental exposure to blood-borne pathogens.
abstract: Acute hepatitis C is known to respond better to interferon therapy than chronic hepatitis C. The reason for this difference remains unclear. The present study was undertaken to examine HCV quasispecies in blood from patients with acute hepatitis C caused by accidental exposure to blood-borne pathogens and in blood from the source patients. Three patients who developed hepatitis C (recipient patients; R-Pt.) and two patients who served as a source of HCV infection (source patients; S-Pt.) were the subjects of this study. The number of quasispecies and the genetic diversity in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence single-strand conformation polymorphism and sequence analysis (FSSA). On the day of the accident, the number of quasispecies and genetic diversity were 13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of diagnosis of acute hepatitis, the number of quasispecies and nucleotide diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3, respectively. Immediately before the start of treatment, the number of quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon therapy resulted in eradication of HCV. These findings indicate that in the early stage of HCV infection, only a portion of HCV transmitted from S-Pts to R-Pts can proliferate. The low number of quasispecies of HCV appears to be one of the reasons why acute hepatitis responds well to interferon therapy.
authors.affiliation: Department of Hepatology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi Abeno-ku, Osaka 545-8585, Japan. takeda@med.osaka-cu.ac.jp
authors.forename: Tadashi
authors.initials: T
authors.lastname: Takeda
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Tatsumi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nakayama
authors.forename: Takahiro
authors.initials: T
authors.lastname: Yasuda
authors.forename: Shuhei
authors.initials: S
authors.lastname: Nishiguchi
authors.forename: Shuichi
authors.initials: S
authors.lastname: Seki
mesh_terms: D000208:Acute Disease; D000328:Adult; D000595:Amino Acid Sequence; D001483:Base Sequence; D017848:Blood-Borne Pathogens; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics* / Q000302:isolation & purification; D006526:Hepatitis C / Q000635:transmission / Q000821:virology*; D006801:Humans; D017758:Infectious Disease Transmission, Patient-to-Professional; D008297:Male; D008969:Molecular Sequence Data; D010564:Personnel, Hospital; D011110:Polymorphism, Genetic; D018807:Polymorphism, Single-Stranded Conformational; D013997:Time Factors; D014764:Viral Proteins / Q000235:genetics*
chemical_list: C400562:HVR1 protein, Hepatitis C virus; D014764:Viral Proteins