title: Effect of GB virus C on response to antiretroviral therapy in HIV-infected Brazilians.
abstract: OBJECTIVE
  GB virus C (GBV-C) infection is associated with delayed mortality in HIV-infected people in most, but not all, studies. Previous investigations of the effect of GBV-C viraemia on response to antiretroviral therapy (ART) were inconclusive. To determine the effect of GBV-C on ART, we retrospectively analysed plasma samples taken from patients in a prospective randomized clinical trial of ART in HIV-positive Brazilians.
  
  
  METHODS
  GBV-C viraemia was characterized by testing stored serum samples from 175 participants by reverse transcriptase-polymerase chain reaction (RT-PCR). Subjects were randomized to receive indinavir (n=59), zidovudine and lamivudine (n=58), or zidovudine, lamivudine and indinavir (n=58). The effect of GBV-C viraemia on the average change in HIV viral load and CD4 count following initiation of therapy was evaluated in a multiple regression analysis.
  
  
  RESULTS
  The prevalence of GBV-C viraemia was similar to that observed in previous studies (24%). HIV viral load decreased following ART to a significantly greater extent in patients with GBV-C viraemia (by 0.48 log(10) HIV-1 RNA copies/mL, P=0.009, adjusting for age, ART group, and baseline CD4 count). Although there was no significant difference in change in CD4 count between individuals with and without GBV-C viraemia overall, CD4 counts were higher following 48 weeks of therapy in GBV-C viraemic individuals receiving the least potent ART regimen (zidovudine and lamivudine) compared with those without GBV-C infection.
  
  
  CONCLUSIONS
  GBV-C viraemia is associated with an enhanced reduction of HIV viral load in response to ART. In this study of treatment-naive individuals during 48 weeks of follow up, patients with GBV-C viraemia had reductions in HIV viral load that were approximately 0.5 log copies/mL greater than those found in patients without GBV-C viraemia. This is similar to reductions observed with nucleoside reverse transcriptase inhibitors.
authors.affiliation: Department of Internal Medicine, University of Iowa Roy, Iowa City, IA 52242, USA.
authors.forename: I E
authors.initials: IE
authors.lastname: Souza
authors.forename: W
authors.initials: W
authors.lastname: Zhang
authors.forename: R S
authors.initials: RS
authors.lastname: Diaz
authors.forename: K
authors.initials: K
authors.lastname: Chaloner
authors.forename: D
authors.initials: D
authors.lastname: Klinzman
authors.forename: J T
authors.initials: JT
authors.lastname: Stapleton
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D004359:Drug Therapy, Combination; D005260:Female; D018178:Flaviviridae Infections / Q000150:complications*; D029407:GB virus C; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000302:isolation & purification; D006801:Humans; D008297:Male; D012367:RNA, Viral / Q000097:blood; D012189:Retrospective Studies; D016896:Treatment Outcome; D019562:Viral Load; D014766:Viremia / Q000150:complications
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral