title: Hepatitis C virus coinfection and HIV load, CD4+ cell percentage, and clinical progression to AIDS or death among HIV-infected women: Women and Infants Transmission Study.
abstract: BACKGROUND
  Despite previous study, it remains unclear whether hepatitis C virus (HCV) coinfection affects the progression of human immunodeficiency virus (HIV) type 1 infection. The Women and Infants Transmission Study provided an opportunity to assess this issue.
  
  
  METHODS
  Longitudinal data on 652 HIV-1-infected women enrolled in the study before the availability of highly active antiretroviral therapy (HAART; 1989-1995) were analyzed. Random effects models were used to determine whether HCV coinfection was associated with different CD4+ cell percentages and HIV-1 RNA levels over time, and Cox proportional hazards models were used to compare the rates of clinical progression to acquired immunodeficiency syndrome (AIDS) or death.
  
  
  RESULTS
  Of 652 women, 190 (29%) were HCV infected. During follow-up, 19% of women were exposed to HAART. After controlling for indicators of disease progression (CD4+ cell percentages and HIV-1 RNA levels determined closest to the time of delivery in pregnant women), ongoing drug use, receipt of antiretroviral therapy, and other important covariates, no differences were detected in the HIV-1 RNA levels, but the CD4+ cell percentages were slightly higher in HCV-infected women than in HCV-uninfected women. During follow-up, 48 women had progression to a first clinical AIDS-defining illness (ADI), and 26 died with no documented antecedent ADI. In multivariable analyses, HCV-infected participants did not have faster progression to a first class C AIDS-defining event or death (relative hazard, 0.75; 95% confidence interval, 0.37-1.53).
  
  
  CONCLUSIONS
  In this cohort, the rate of clinical progression of HIV-1 infection was not greater for HCV-infected women.
authors.affiliation: University of Illinois at Chicago School of Public Health, Chicago, IL 60612, USA. rchersho@uic.edu
authors.forename: Ronald C
authors.initials: RC
authors.lastname: Hershow
authors.forename: Peter T
authors.initials: PT
authors.lastname: O'Driscoll
authors.forename: Ed
authors.initials: E
authors.lastname: Handelsman
authors.forename: Jane
authors.initials: J
authors.lastname: Pitt
authors.forename: George
authors.initials: G
authors.lastname: Hillyer
authors.forename: Leslie
authors.initials: L
authors.lastname: Serchuck
authors.forename: Ming
authors.initials: M
authors.lastname: Lu
authors.forename: Katherine T
authors.initials: KT
authors.lastname: Chen
authors.forename: Sigal
authors.initials: S
authors.lastname: Yawetz
authors.forename: Susan
authors.initials: S
authors.lastname: Pacheco
authors.forename: Katherine
authors.initials: K
authors.lastname: Davenny
authors.forename: Samuel
authors.initials: S
authors.lastname: Adeniyi-Jones
authors.forename: David L
authors.initials: DL
authors.lastname: Thomas
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* / Q000276:immunology / Q000401:mortality / Q000821:virology*; D006526:Hepatitis C / Q000150:complications* / Q000453:epidemiology / Q000276:immunology* / Q000821:virology; D018937:Hepatitis C Antibodies / Q000097:blood; D006801:Humans; D016016:Proportional Hazards Models; D012367:RNA, Viral / Q000097:blood; D019966:Substance-Related Disorders; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D018937:Hepatitis C Antibodies; D012367:RNA, Viral