title: GB virus C (GBV-C) infection in hepatitis C virus (HCV)/HIV-coinfected patients receiving HCV treatment: importance of the GBV-C genotype.
abstract: BACKGROUND
  Persistent GB virus C (GBV-C) coinfection leads to slower human immunodeficiency virus (HIV) progression. Despite the existence of multiple GBV-C genotypes, their relevance to the progression of HIV disease is unknown. We therefore investigated (1) the prevalence and genotype of GBV-C in hepatitis C virus (HCV)/HIV-coinfected patients and (2) the impact of HCV treatment on GBV-C RNA clearance.
  
  
  METHODS
  We retrospectively studied 130 HCV/HIV-coinfected patients initiating HCV therapy. Anti-E2 enzyme-linked immunosorbent assay, reverse-transcription polymerase chain reaction (PCR), and real-time PCR were used to detect and quantify GBV-C infection. GBV-C genotype was determined by sequencing the 5' untranslated region.
  
  
  RESULTS
  GBV-C infection (past or current) was identified in 111 (85%) of the patients. Ongoing GBV-C replication was detected in 40 patients. Coinfection with GBV-C genotype 2 was associated with significantly higher CD4(+) cell counts. After 24 weeks of HCV therapy, GBV-C RNA clearance was observed in 50% of patients, although this was not associated with changes in HIV load or with CD4(+) cell counts. Sustained GBV-C RNA clearance was observed in 31% of patients with GBV-C RNA detected at baseline.
  
  
  CONCLUSIONS
  GBV-C coinfection was extremely common. GBV-C RNA clearance with HCV therapy was associated with neither short-term loss of HIV control nor impaired immune status. The association of GBV-C genotype 2 with higher CD4(+) cell counts merits further study.
authors.affiliation: Department of Internal Medicine I, University of Bonn, Bonn, Germany.
authors.forename: Carolynne
authors.initials: C
authors.lastname: Schwarze-Zander
authors.forename: Jason T
authors.initials: JT
authors.lastname: Blackard
authors.forename: Hui
authors.initials: H
authors.lastname: Zheng
authors.forename: Marylyn M
authors.initials: MM
authors.lastname: Addo
authors.forename: Wenyu
authors.initials: W
authors.lastname: Lin
authors.forename: Gregory K
authors.initials: GK
authors.lastname: Robbins
authors.forename: Kenneth E
authors.initials: KE
authors.lastname: Sherman
authors.forename: Dietmar
authors.initials: D
authors.lastname: Zdunek
authors.forename: Georg
authors.initials: G
authors.lastname: Hess
authors.forename: Raymond T
authors.initials: RT
authors.lastname: Chung
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000494:pharmacology / Q000627:therapeutic use; D018791:CD4 Lymphocyte Count; D005260:Female; D029407:GB virus C / Q000235:genetics* / Q000302:isolation & purification; D005838:Genotype; D015658:HIV Infections / Q000150:complications*; D006526:Hepatitis C / Q000150:complications / Q000188:drug therapy / Q000453:epidemiology / Q000821:virology; D006525:Hepatitis, Viral, Human / Q000150:complications / Q000453:epidemiology* / Q000821:virology; D006801:Humans; D007372:Interferons / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008404:Massachusetts / Q000453:epidemiology; D015995:Prevalence; D012367:RNA, Viral / Q000032:analysis / Q000187:drug effects; D012189:Retrospective Studies; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000998:Antiviral Agents; D012367:RNA, Viral; D007372:Interferons