title: Predictors of suboptimal CD4 response among women achieving virologic suppression in a randomized antiretroviral treatment trial, Africa.
abstract: BACKGROUND
  A subset of HIV-1 infected patients starting highly active antiretroviral treatment (HAART) experience suboptimal CD4 response (SCR) despite virologic suppression. We studied the rate of and risk factors for SCR among women starting HAART in the ACTG A5208 study conducted in 7 African countries. 741 HAART-naive women with screening CD4 count <200 cells/μL were randomized to start HAART with Tenofovir/Emtricitabine plus either Nevirapine or Lopinavir/Ritonavir.
  
  
  METHODS
  This analysis includes the 625 women who remained on-study through 48 weeks without experiencing protocol-defined virologic failure. We defined SCR as<100 CD4 cells/μL increase from baseline and absolute CD4 cell count<350 cells/μL, both at 48 weeks after HAART initiation.
  
  
  RESULTS
  The baseline characteristics for the 625 women prior to HAART initiation were: median age 33 years, screening CD4 count 134 cells/μL, and HIV-1 RNA 5.1 log10 copies/mL; 184 (29%) were WHO Stage 3 or 4.Seventy one (11%) of these 625 women experienced SCR. Baseline factors independently associated with increased odds of SCR included older age, lower HIV-1 RNA, positive Hepatitis B surface antigen, and site location. At 96 weeks, only 6% of the SCR group had CD4 ≥ 350 cells/μL compared with 67% in the non SCR group.
  
  
  CONCLUSIONS
  After starting HAART, 11% of women with virologic suppression through 48 weeks experienced SCR. These patients were also less likely to achieve CD4 ≥ 350 cells/μL by 96 weeks. The underlying causes and long term clinical implications of SCR deserve further investigation.
  
  
  BACKGROUND
  Clinicaltrials.gov Identifier: NCT00089505.
authors.affiliation: Botswana Harvard School of Public Health AIDS Initiative Partnership, Gaborone, Botswana. aasmelash@bhp.org.bw.
authors.forename: Aida
authors.initials: A
authors.lastname: Asmelash
authors.forename: Yu
authors.initials: Y
authors.lastname: Zheng
authors.forename: Kara Wools
authors.initials: KW
authors.lastname: Kaloustian
authors.forename: Douglas
authors.initials: D
authors.lastname: Shaffer
authors.forename: Fred
authors.initials: F
authors.lastname: Sawe
authors.forename: Anthony
authors.initials: A
authors.lastname: Ogwu
authors.forename: Robert
authors.initials: R
authors.lastname: Salata
authors.forename: Judith
authors.initials: J
authors.lastname: Currier
authors.forename: Michael D
authors.initials: MD
authors.lastname: Hughes
authors.forename: Shahin
authors.initials: S
authors.lastname: Lockman
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000328:Adult; D000349:Africa; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000068679:Emtricitabine; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D061466:Lopinavir / Q000627:therapeutic use; D019829:Nevirapine / Q000627:therapeutic use; D063065:Organophosphonates / Q000627:therapeutic use; D019438:Ritonavir / Q000627:therapeutic use; D000068698:Tenofovir; D016896:Treatment Outcome
chemical_list: D019380:Anti-HIV Agents; D063065:Organophosphonates; D003841:Deoxycytidine; D061466:Lopinavir; D019829:Nevirapine; D000068698:Tenofovir; D000068679:Emtricitabine; D000225:Adenine; D019438:Ritonavir