title: Influence of hepatitis C virus infection on HIV-1 disease progression and response to highly active antiretroviral therapy.
abstract: OBJECTIVE
  To assess hepatitis C virus (HCV) antibody prevalence in the EuroSIDA cohort, along with survival, human immunodeficiency virus (HIV)-1 disease progression, virologic response (plasma HIV-1 RNA load of < 500 copies/mL), and CD4 cell count recovery by HCV serostatus in patients initiating highly active antiretroviral therapy (HAART).
  
  
  RESULTS
  HCV serostatus at or before enrollment was available for 5957 patients; 1960 (33%) and 3997 (67%) were HCV seropositive and seronegative, respectively. No association between an increased incidence of acquired immunodeficiency syndrome-defining illnesses or death and HCV serostatus was seen after adjustment for other prognostic risk factors known at baseline (adjusted incidence rate ratio [IRR], 0.97 [95% confidence interval {CI}, 0.81-1.16]). However, there was a large increase in the incidence of liver disease-related deaths in HCV-seropositive patients in adjusted models (IRR, 11.71 [95% CI, 6.42-21.34]). Among 2260 patients of known HCV serostatus initiating HAART, after adjustment, there was no significant difference between HCV-seropositive and -seronegative patients with respect to virologic response (relative hazard [RH], 1.13 [95% CI, 0.84-1.51]) and immunologic response, whether measured as a > or = 50% increase (RH, 0.94 [95% CI, 0.77-1.16]) or a > or = 50 cells/microL increase (RH, 0.92 [95% CI, 0.77-1.11]) in CD4 cell count after HAART initiation.
  
  
  CONCLUSIONS
  HCV serostatus did not affect the risk of HIV-1 disease progression, but the risk of liver disease-related deaths was markedly increased in HCV-seropositive patients. The overall virologic and immunologic responses to HAART were not affected by HCV serostatus.
authors.affiliation: Department of Medicine I, University Hospital Bonn, Bonn, Germany. juergen.rockstroh@ukb.uni-bonn.de
authors.forename: Jürgen K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: Amanda
authors.initials: A
authors.lastname: Mocroft
authors.forename: Vincent
authors.initials: V
authors.lastname: Soriano
authors.forename: Cristina
authors.initials: C
authors.lastname: Tural
authors.forename: Marcello H
authors.initials: MH
authors.lastname: Losso
authors.forename: Andrzej
authors.initials: A
authors.lastname: Horban
authors.forename: Ole
authors.initials: O
authors.lastname: Kirk
authors.forename: Andrew
authors.initials: A
authors.lastname: Phillips
authors.forename: Bruno
authors.initials: B
authors.lastname: Ledergerber
authors.forename: Jens
authors.initials: J
authors.lastname: Lundgren
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000302:isolation & purification; D006526:Hepatitis C / Q000150:complications* / Q000276:immunology / Q000401:mortality; D018937:Hepatitis C Antibodies / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D012307:Risk Factors; D016019:Survival Analysis
chemical_list: D019380:Anti-HIV Agents; D018937:Hepatitis C Antibodies; D012367:RNA, Viral