title: Clinical presentation of GB-C virus infection in drug abusers with chronic hepatitis C.
abstract: OBJECTIVE
  Recently, the hepatitis GB-C virus (GBV-C) has been identified as another virus potentially causing chronic hepatitis. Although high rates of coinfection are emerging in drug addicts with chronic hepatitis C virus infection, no detailed data on clinical presentation are available. Therefore, co-infection was sought in hepatitis C virus patients to determine the impact of GB-C virus on clinical presentation.
  
  
  METHODS
  GBV-C was determined by nested reverse transcriptase-polymerase chain reaction in serum of 70 HIV negative intravenous drug abusers with chronic hepatitis C. Biochemical, histological and virological parameters were compared between patients with or without GBV-C coinfection.
  
  
  RESULTS
  Hepatitis C virus and GBV-C coinfection was found in 18 of 70 (25.7%) patients. Cases with coinfection were younger and had shorter duration of disease (31.4+/-6.2 vs. 35.3+/-7.3 (p=0.09) and 9.9+/-6.8 vs. 12.9+/-7.7 (p=0.17) years) than those without coinfection. Neither hepatitis C virus genotype distribution and HCV RNA levels nor serum liver function tests, titers of immunoglobulins or autoantibodies differed between the two groups. Histologically, chronic active hepatitis (16.7 vs. 46.4%, p=0.07), fibrosis (8.3% vs. 21.4%, p=0.3), and cirrhosis (0% vs. 8.2%, p=0.31) were less prevalent in coinfected patients. After interferon treatment, 5/6 coinfected and 11/19 patients with hepatitis C virus infection alone had cleared HCV RNA and 4/6 lost GBV-C RNA from serum. The two patients with GBV-C/HCV infection who persistently cleared hepatitis C virus but not GBV-C from serum had normal transaminases during follow-up despite persistence of GBV-C.
  
  
  CONCLUSIONS
  Coinfection of chronic hepatitis C patients with GBV-C does not lead to a significant change in clinical presentation, severity of liver disease, hepatitis C viremia, or response to interferon treatment.
authors.affiliation: Department of Internal Medicine, University of Heidelberg, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Goeser
authors.forename: S
authors.initials: S
authors.lastname: Seipp
authors.forename: R
authors.initials: R
authors.lastname: Wahl
authors.forename: H M
authors.initials: HM
authors.lastname: Müller
authors.forename: W
authors.initials: W
authors.lastname: Stremmel
authors.forename: L
authors.initials: L
authors.lastname: Theilmann
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000974:Antibodies, Antinuclear / Q000032:analysis; D000998:Antiviral Agents / Q000627:therapeutic use; D002908:Chronic Disease; D017931:DNA Primers / Q000737:chemistry; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D018067:Flaviviridae / Q000235:genetics* / Q000276:immunology; D005500:Follow-Up Studies; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics* / Q000276:immunology; D006526:Hepatitis C / Q000150:complications* / Q000473:pathology / Q000628:therapy; D018937:Hepatitis C Antibodies / Q000032:analysis; D006525:Hepatitis, Viral, Human / Q000150:complications* / Q000473:pathology / Q000628:therapy; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D008297:Male; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000032:analysis*; D012189:Retrospective Studies; D015819:Substance Abuse, Intravenous / Q000097:blood / Q000150:complications* / Q000821:virology
chemical_list: D000974:Antibodies, Antinuclear; D000998:Antiviral Agents; D017931:DNA Primers; D018937:Hepatitis C Antibodies; D016898:Interferon-alpha; D012367:RNA, Viral; D000410:Alanine Transaminase