title: Prevalence of genotypic and phenotypic HIV-1 drug-resistant strains among patients who have rebound in viral load while receiving antiretroviral therapy in the UNAIDS-Drug Access Initiative in Abidjan, Côte d'Ivoire.
abstract: OBJECTIVE
  To determine the prevalence of genotypic and phenotypic antiretroviral (ARV) drug-resistant HIV-1 strains among patients with viral load rebound while receiving ARV therapy in Abidjan, Côte d'Ivoire.
  
  
  METHODS
  Between August 1998 and April 2000, we selected all patients (n = 241) who had received ARV drug therapy for at least 6 months in the UNAIDS-Drug Access Initiative (DAI), in Abidjan. We analyzed for genotypic and phenotypic drug resistance among 97 (40%) of the 241 patients who had a rebound in plasma viral load, defined as an initial decrease of > 0.5 log10 copies/ml followed by a subsequent increase of > 0.25 log10 copies/ml.
  
  
  RESULTS
  Of the viruses isolated from the 97 patients, 86 (88.7%) had usable sequences and 68 (79%) of the 86 patients had genotypic resistance to at least one reverse transcriptase inhibitor (RTI) or protease inhibitor (PI). Resistant mutations were found for zidovudine in 50 (78%) of 64 patients who had received the drug, 11 (68.7%) of 16 patients on lamivudine, for nevirapine in two (2%), for indinavir in one (1%), and for ritonavir in one (1%). Phenotypic resistance to at least one nucleoside RTI was seen in 45 (56%) of the 80 patients tested, to non-nucleoside RTIs in eight (10%), and to PIs in one (1.3%). Multivariate regression analysis showed factors associated with resistance to be initial treatment with dual therapy (P = 0.04) compared with highly active antiretroviral therapy, and maximal initial viral load response (P = 0.006).
  
  
  CONCLUSIONS
  Our results demonstrate a high prevalence of ARV drug resistance associated with dual ARV therapy. These results indicate the limited role for dual ARV therapy.
authors.affiliation: Projet RETRO-CI, Abidjan, Côte d'Ivoire.
authors.forename: Christiane
authors.initials: C
authors.lastname: Adjé-Touré
authors.forename: Bilé
authors.initials: B
authors.lastname: Celestin
authors.forename: Debra
authors.initials: D
authors.lastname: Hanson
authors.forename: Thierry H
authors.initials: TH
authors.lastname: Roels
authors.forename: Kurt
authors.initials: K
authors.lastname: Hertogs
authors.forename: Brendan
authors.initials: B
authors.lastname: Larder
authors.forename: Fabien
authors.initials: F
authors.lastname: Diomande
authors.forename: Martine
authors.initials: M
authors.lastname: Peeters
authors.forename: Serge
authors.initials: S
authors.lastname: Eholié
authors.forename: Eve
authors.initials: E
authors.lastname: Lackritz
authors.forename: Terence
authors.initials: T
authors.lastname: Chorba
authors.forename: John N
authors.initials: JN
authors.lastname: Nkengasong
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D007560:Cote d'Ivoire; D003906:Developing Countries; D024921:Drug Resistance, Multiple, Viral / Q000235:genetics*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D017320:HIV Protease Inhibitors / Q000627:therapeutic use; D054303:HIV Reverse Transcriptase / Q000037:antagonists & inhibitors; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D016015:Logistic Models; D008297:Male; D009154:Mutation; D010641:Phenotype; D015995:Prevalence; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D054303:HIV Reverse Transcriptase