title: Hepatitis G virus infection markers (RNA and anti-E2 antibodies) in a multicenter cohort of hemophiliacs.
abstract: OBJECTIVE
  To investigate the prevalence and evolution of hepatitis G virus (HGV) infection in hemophiliacs and to correlate evolution of HGV infection markers with immunologic parameters in those patients co-infected with HIV.
  
  
  METHODS
  HGV RNA and anti-E2 antibodies were studied in 124 patients. Serial samples were drawn every 4 months from 1992 to 1996. Lymphocyte subsets including T-helper lymphocytes, T-suppressor lymphocytes, T-cytotoxic lymphocytes, activated T-lymphocytes and natural killer cells were analyzed.
  
  
  RESULTS
  Prevalences were 22.6% for HGV RNA and 18.5% for anti-E2. Four patients had both HGV RNA and anti E2, so the overall prevalence of HGV infection in hemophiliacs was 37.9% (11.5% in 200 controls, p<0.0001). After a median follow-up of 36.6 months 20 patients remained HGV RNA positive, whereas HGV RNA had cleared in 8, with an actuarial probability of clearance at 36 months of 34.6%. Only 2 patients developed anti-E2 antibodies. Four patients cleared anti-E2, with an actuarial probability at 36 months of 24.8%. In patients with HIV infection, both lower CD4+ lymphocyte count (p=0.01) or higher CD8+ lymphocyte count (p=0.03) showed predictive value for probability of clearing HGV-RNA. CD4+/CD8+ ratio (p=0.002) was the only variable included in the best model for HGV-RNA disappearance.
  
  
  CONCLUSIONS
  A more accurate estimation of the prevalence of HGV infection can be achieved with the determination of both HGV RNA and anti-E2. Anti-E2 response can be undetectable or transitory after disappearance of HGV-RNA, giving therefore rise to the possibility of underestimating HGV prevalence with currently diagnostic methods. In HIV-positive patients, cellular immune function seems to be involved in the resolution of HGV infection, following the significant correlation found between clearance of HGV-RNA and CD4+/CD8+ lymphocyte populations.
authors.affiliation: Service of Hemotherapy and Hemostasis, Hospital Clínic Villarroel 170, 08036 Barcelona, Spain. dtassies@medicina.ub.es
authors.forename: D
authors.initials: D
authors.lastname: Tàssies
authors.forename: M
authors.initials: M
authors.lastname: Magallón
authors.forename: M
authors.initials: M
authors.lastname: Quintana
authors.forename: R P
authors.initials: RP
authors.lastname: Fernández-Urgellés
authors.forename: C
authors.initials: C
authors.lastname: Rodriguez-Pinto
authors.forename: J
authors.initials: J
authors.lastname: Tusell
authors.forename: C
authors.initials: C
authors.lastname: Altisent
authors.forename: J C
authors.initials: JC
authors.lastname: Reverter
authors.forename: R
authors.initials: R
authors.lastname: Mazzara
authors.forename: A
authors.initials: A
authors.lastname: Ordinas
authors.forename: J
authors.initials: J
authors.lastname: Monteagudo
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers; D015331:Cohort Studies; D005260:Female; D018067:Flaviviridae; D005500:Follow-Up Studies; D015483:HIV Antibodies / Q000097:blood*; D015658:HIV Infections / Q000209:etiology / Q000821:virology; D006467:Hemophilia A / Q000097:blood / Q000821:virology*; D006525:Hepatitis, Viral, Human / Q000235:genetics* / Q000276:immunology*; D006801:Humans; D016131:Lymphocyte Subsets / Q000821:virology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood*; D013030:Spain / Q000453:epidemiology; D013997:Time Factors; D014759:Viral Envelope Proteins / Q000276:immunology
chemical_list: D015415:Biomarkers; D015483:HIV Antibodies; D012367:RNA, Viral; D014759:Viral Envelope Proteins