title: Clinical implications of GBV-C/HGV infection in patients with "HCV-related" chronic hepatitis.
abstract: OBJECTIVE
  To evaluate the clinical, biochemical and histological implications of a concomitant HGV infection in "HCV-related" chronic liver disease.
  
  
  METHODS
  Eighty-three HCV-RNA positive patients with chronic liver disease were tested for GBV-C/HGV coinfection by heminested PCR.
  
  
  RESULTS
  Twenty-two (26.5%) patients were found to be positive for GBV-C/HGV RNA. GBV-C/HGV+ patients differed significantly from GBV-C/HGV- ones for younger age, higher frequency of history of drug addiction, which in turn might favor coinfection with interferon-sensitive HCV genotypes (3a), and increased probability of long-term response to interferon. GBV-C/HGV infection appears to have no responsibility for specific aspects of HCV infection such as biochemical or histological cholestatic features, lymphoid follicles, symptomatic cryoglobulinemia or presence of serum autoantibodies, including LKM1. It does not worsen the HCV-related disease (ALT levels and histological activity) and does not significantly interfere with HCV infection, as explored by the number of hepatocytes positive for HCV antigens. The amount of steatosis (mean score) was shown to be higher in GBV-C/HGV+ patients. A virological follow up was performed in 17 interferon-treated GBV-C/HGV+ patients On the whole, GBV-C/HGV seems to be as sensitive to IFN treatment as HCV, but recurrence after withdrawal is more frequent. In spite of this, ALT levels often remain normal after treatment withdrawal.
  
  
  CONCLUSIONS
  The present data suggest that GBV-C/HGV infection, apart from more marked liver steatosis, does not modify the overall picture of chronic hepatitis due to HCV infection.
authors.affiliation: Servizio di Semeiotica Medica II, Azienda Ospedaliera, Università degli Studi, Bologna, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Francesconi
authors.forename: F
authors.initials: F
authors.lastname: Giostra
authors.forename: G
authors.initials: G
authors.lastname: Ballardini
authors.forename: A
authors.initials: A
authors.lastname: Manzin
authors.forename: L
authors.initials: L
authors.lastname: Solforosi
authors.forename: F
authors.initials: F
authors.lastname: Lari
authors.forename: C
authors.initials: C
authors.lastname: Descovich
authors.forename: S
authors.initials: S
authors.lastname: Ghetti
authors.forename: A
authors.initials: A
authors.lastname: Grassi
authors.forename: G
authors.initials: G
authors.lastname: Bianchi
authors.forename: D
authors.initials: D
authors.lastname: Zauli
authors.forename: M
authors.initials: M
authors.lastname: Clementi
authors.forename: F B
authors.initials: FB
authors.lastname: Bianchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D001706:Biopsy; D005260:Female; D018067:Flaviviridae; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification; D006508:Hepatitis Antibodies / Q000097:blood*; D006526:Hepatitis C / Q000150:complications* / Q000473:pathology / Q000628:therapy; D018936:Hepatitis C Antigens / Q000032:analysis; D006525:Hepatitis, Viral, Human / Q000150:complications* / Q000473:pathology / Q000628:therapy; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D008099:Liver / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies; D019966:Substance-Related Disorders
chemical_list: D006508:Hepatitis Antibodies; D018936:Hepatitis C Antigens; D012367:RNA, Viral; D007372:Interferons