title: Response to interferon of GB virus C and hepatitis C virus in patients with chronic hepatitis.
abstract: OBJECTIVE
  To evaluate the response to interferon and capacity to induce liver disease of a putative non-A to E hepatitis virus designated GB virus C (GBV-C).
  
  
  METHODS
  RNA of GBV-C was detected by reverse transcription polymerase chain reaction with nested primers deduced from the 5'-noncoding region. It was titrated, along with RNA of hepatitis C virus (HCV), in 16 co-infected patients (11%) out of 140 patients who received interferon.
  
  
  RESULTS
  At the completion of a 6-month course of interferon (total dose: 516-774 million units), GBV-C RNA disappeared from serum in seven (44%) and HCV RNA from serum in 11 (69%) patients. At 6 months after interferon treatment ended, GBV-C RNA remained cleared in three patients (19%), and HCV RNA was persistently undetectable in four (25%). One patient lost both GBV-C and HCV RNAs. The three patients whose serum was cleared of GBV-C RNA had pretreatment titers of the virus (two with 10[1]/ml and one with 10[2]/ml) that were considerably lower than the titers of 13 patients (one with 10[2]/ml, eight with 10[3]/ml, and four with > or = 10[4]/ml) without such clearance. The decrease in alanine aminotransferase levels paralleled the response of HCV RNA but not that of GBV-C RNA to interferon. The response of HCV at 6 months after interferon in the co-infected patients (4/16 or 25%) did not differ significantly from that in patients without GBV-C infection (44/124 or 35%).
  
  
  CONCLUSIONS
  The sensitivity of GBV-C to interferon is comparable to but independent of HCV. Co-infection with GBV-C does not influence the response to interferon of patients with chronic hepatitis C.
authors.affiliation: First Department of Internal Medicine, Yamanashi Medical University, Yamanashi-Ken, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Sakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Akahane
authors.forename: H
authors.initials: H
authors.lastname: Okamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Miyakawa
authors.forename: M
authors.initials: M
authors.lastname: Mayumi
mesh_terms: D000998:Antiviral Agents / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D004341:Drug Evaluation; D005260:Female; D018067:Flaviviridae / Q000235:genetics; D005838:Genotype; D015483:HIV Antibodies / Q000097:blood; D016174:Hepacivirus / Q000235:genetics; D006510:Hepatitis B Antibodies / Q000097:blood; D018937:Hepatitis C Antibodies / Q000097:blood; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology / Q000628:therapy*; D006525:Hepatitis, Viral, Human / Q000097:blood / Q000276:immunology / Q000628:therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage*; D008297:Male; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012189:Retrospective Studies; D013997:Time Factors
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D015483:HIV Antibodies; D006510:Hepatitis B Antibodies; D018937:Hepatitis C Antibodies; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins