title: Interferon-alpha therapy in patients dually infected with hepatitis C virus and GB virus C/hepatitis G virus--virological response of HGV and pretreatment HGV viremia level.
abstract: OBJECTIVE
  The response to interferon-alpha (IFN) therapy of recently isolated GB virus C and hepatitis G virus (HGV) is still unclear. To investigate the biochemical and virological response to IFN therapy in patients with chronic hepatitis C virus (HCV) infection concomitantly infected with HGV, 196 patients with HCV who had received IFN therapy were retrospectively studied.
  
  
  METHODS
  HGV and HCV RNA were detected by reverse transcription nested polymerase chain reaction (RT-PCR). Serum HGV RNA levels were quantified by competitive RT-PCR. The HGV genotype was detected by restriction fragment length polymorphism analysis using the PCR products.
  
  
  RESULTS
  Of 196 patients, 16 (8.2%) were positive for both HCV and HGV RNA before IFN therapy. There were no significant clinical and virological differences between the patients with dual infection and those with only HCV infection. During the therapy, a decrease or loss of serum HGV RNA level was observed in these patients. Six months after cessation of the therapy, five of 16 patients became negative for HGV RNA by RT-PCR. The pretreatment HGV RNA level of the patients who lost HGV RNA after cessation of IFN was low (median=10(3) copies/ml), compared to the level (median=10(7) copies/ml, p<0.01) in the patients with positive HGV RNA after the therapy. The HGV genotype of these 16 patients was the same type.
  
  
  CONCLUSIONS
  These data suggest that: 1) there is no significant difference in response to IFN therapy between patients with dual and single infection; 2) HGV shows sensitivity to IFN therapy; and 3) in the patients who show a low pretreatment HGV RNA level, serum HGV RNA becomes undetectable by RT-PCR after cessation of IFN therapy.
authors.affiliation: Second Department of Medicine, Nagoya City University, Medical School, Nagoya, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Orito
authors.forename: M
authors.initials: M
authors.lastname: Mizokami
authors.forename: K
authors.initials: K
authors.lastname: Yasuda
authors.forename: K
authors.initials: K
authors.lastname: Sugihara
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Mukaide
authors.forename: K I
authors.initials: KI
authors.lastname: Ohba
authors.forename: T
authors.initials: T
authors.lastname: Nakano
authors.forename: T
authors.initials: T
authors.lastname: Kato
authors.forename: Y
authors.initials: Y
authors.lastname: Kondo
authors.forename: T
authors.initials: T
authors.lastname: Kumada
authors.forename: R
authors.initials: R
authors.lastname: Ueda
authors.forename: S
authors.initials: S
authors.lastname: Iino
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D018067:Flaviviridae; D005838:Genotype; D006526:Hepatitis C / Q000188:drug therapy*; D006525:Hepatitis, Viral, Human / Q000188:drug therapy*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction / Q000379:methods; D012189:Retrospective Studies; D015163:Superinfection / Q000188:drug therapy; D014158:Transcription, Genetic; D014766:Viremia / Q000188:drug therapy*
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha