title: Plasma HIV viral load in patients with hemophilia and late-stage HIV disease: a measure of current immune suppression. Multicenter Hemophilia Cohort Study.
abstract: BACKGROUND
  For patients infected with HIV, plasma HIV viral load in early disease predicts long-term prognosis. However, the implications of viral load measurements late in HIV disease are uncertain.
  
  
  OBJECTIVE
  To evaluate the relation between plasma HIV viral load and subsequent risk for disease progression in patients with late-stage HIV disease.
  
  
  METHODS
  Retrospective cohort study.
  
  
  METHODS
  16 treatment centers for patients with hemophilia.
  
  
  METHODS
  389 patients with hemophilia and late-stage HIV disease (CD4 count < 200 cells/mm3).
  
  
  METHODS
  Plasma HIV viral load was measured at baseline. Patients were followed for AIDS-related illnesses (primary outcome) and, specifically, Pneumocystis carinii pneumonia (secondary outcome).
  
  
  RESULTS
  HIV viral load strongly predicted AIDS-related illness. For patients with viral loads less than 4.00 log10 copies/mL, the 1-year actuarial risk was 0% and the 5-year risk was 25%. For patients with viral loads of at least 6.00 log10 copies/mL, the 1-year actuarial risk was 42% and the 5-year risk was 78%. A linear relation existed between viral load and risk for AIDS-related illness (hazard ratio, 2.37 per 1og10 copies/mL; P < 0.001). In addition, viral load most strongly predicted risk for illness immediately after viral load testing; this predictive relation attenuated over time (P = 0.002). These findings changed little after adjustment for CD4 cell counts that were updated during follow-up. In the first year after viral load was measured, it predicted occurrence of P. carinii pneumonia (hazard ratio, 4.69 per 1og10 copies/mL; P < 0.001).
  
  
  CONCLUSIONS
  In patients with hemophilia and late-stage HIV disease, viral load predicts disease progression independently of CD4 cell counts. Because viral load most strongly predicts progression immediately after load is measured, it seems to reflect the current level of immunosuppression.
authors.affiliation: Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20822, USA. engelse@exchange.nih.gov
authors.forename: E A
authors.initials: EA
authors.lastname: Engels
authors.forename: P S
authors.initials: PS
authors.lastname: Rosenberg
authors.forename: T R
authors.initials: TR
authors.lastname: O'Brien
authors.forename: J J
authors.initials: JJ
authors.lastname: Goedert
mesh_terms: D017088:AIDS-Related Opportunistic Infections; D000328:Adult; D018791:CD4 Lymphocyte Count; D018450:Disease Progression; D006678:HIV / Q000235:genetics; D015658:HIV Infections / Q000150:complications* / Q000276:immunology*; D006467:Hemophilia A / Q000150:complications*; D006801:Humans; D008297:Male; D015999:Multivariate Analysis; D011020:Pneumonia, Pneumocystis; D011379:Prognosis; D016016:Proportional Hazards Models; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies; D016019:Survival Analysis; D019562:Viral Load
chemical_list: D012367:RNA, Viral