title: Low rate of genotypic HIV-1 drug-resistant strains in the Senegalese government initiative of access to antiretroviral therapy.
abstract: OBJECTIVE
  To monitor the prevalence of antiretroviral (ARV)-resistant HIV-1 viruses, and the genotypic mutations in patients enrolled in the Senegalese initiative for access to antiretroviral treatment (ART).
  
  
  METHODS
  A total of 80 patients with a virological follow-up of at least 6 months were selected, 68 were ART-naive and 12 ART-experienced. Genotypic resistance to ARV was studied at baseline for a random subset of patients and at each rebound in plasma viral load during ART, by sequencing the protease and reverse transcriptase genes.
  
  
  RESULTS
  At baseline, 66 patients received highly active antiretroviral therapy (HAART) [2 nucleoside reverse transcriptase inhibitors (NRTIs) +1 protease inhibitor (PI) (n = 64) or 2 NRTIs + 1 non-nucleoside reverse transcriptase inhibitor (NNRTI) (n = 2)] and 14 patients (17.5%) started with a dual therapy because of ongoing antitubercular therapy or efficient previous bitherapy for the ART-experienced patients. The emergence of drug-resistant viruses (n = 13) during follow-up was more frequent in ART-experienced patients than in ART-naive patients, 41.7 versus 11.8%, resistant viruses emerged at comparable follow-up periods, a median of 17.8 and 18.3 months, respectively. In patients receiving zidovudine and lamivudine in their drug regimen, resistance to lamivudine was more frequent than to zidovudine. Two of the three patients, with viruses resistant to PIs, acquired mutations associated with cross-resistance. Strikingly, five (39%) of the 13 patients developed resistances to drugs that they had never received (n = 3) or that they received 18 or 36 months ago (n = 2). Didanosine/stavudine pressure had selected zidovudine-resistant viruses in four patients, and indinavir had selected a nelfinavir-resistant virus in one patient.
  
  
  CONCLUSIONS
  In contrast to other reports from developing countries where patients had received ARVs in an uncontrolled manner, our study showed that implementation of HAART together with good clinical, biological and logistical monitoring can reduce the emergence of resistant strains in Africa.
authors.affiliation: Institut de Recherche pour le Développement (IRD, UR 36), University of Montpellier, France.
authors.forename: Laurence
authors.initials: L
authors.lastname: Vergne
authors.forename: Coumba Touré
authors.initials: CT
authors.lastname: Kane
authors.forename: Christian
authors.initials: C
authors.lastname: Laurent
authors.forename: Ndella
authors.initials: N
authors.lastname: Diakhaté
authors.forename: Ndeye Fatou Ngom
authors.initials: NF
authors.lastname: Gueye
authors.forename: Pape Mandoumbé
authors.initials: PM
authors.lastname: Gueye
authors.forename: Papa Salif
authors.initials: PS
authors.lastname: Sow
authors.forename: Mame Awa
authors.initials: MA
authors.lastname: Faye
authors.forename: Florian
authors.initials: F
authors.lastname: Liégeois
authors.forename: Adama
authors.initials: A
authors.lastname: Ndir
authors.forename: Isabelle
authors.initials: I
authors.lastname: Lanièce
authors.forename: Martine
authors.initials: M
authors.lastname: Peeters
authors.forename: Ibrahima
authors.initials: I
authors.lastname: Ndoye
authors.forename: Souleymane
authors.initials: S
authors.lastname: Mboup
authors.forename: Eric
authors.initials: E
authors.lastname: Delaporte
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D003906:Developing Countries; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D012367:RNA, Viral / Q000097:blood; D012675:Senegal; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral