title: High prevalence of genotypic and phenotypic HIV-1 drug-resistant strains among patients receiving antiretroviral therapy in Abidjan, Côte d'Ivoire.
abstract: To describe prevalence of antiretroviral (ARV) drug-resistant HIV-1 strains among patients with a history of earlier treatment with ARV drugs in Abidjan, Côte d'Ivoire, we determined mutations that confer HIV-1 ARV drug resistance by sequencing the viral reverse-transcriptase and protease genes derived from plasma viral RNA of 68 individuals consecutively enrolled in the Joint United Nations Program on AIDS Drug Access Initiative (UNAIDS-DAI) with a history of earlier ARV drug treatment in Abidjan between August 1998 and April 1999. Phenotypic ARV drug resistance was assessed using a recombinant virus assay. Primary mutations associated with ARV drug resistance to at least one of the reverse-transcriptase inhibitors or protease inhibitors were detected in 39 (57.4%) of the 68 patients. The prevalence of mutations associated with resistance to ARV drugs was: 29 (42.6%) to zidovudine, 10 (14.7%) to lamivudine, one (1.5%) to didanosine, one K103N mutation (associated with resistance to delavirdine, nevirapine, and efavirenz), one Y181C mutation (associated with resistance to delavirdine and nevirapine), two to both indinavir (M46I/L and V82A) and saquinavir (G48V and L90M), and one each to ritonavir (V82A) and nelfinavir (D30N). Phenotypic resistance to at least one nucleoside reverse transcriptase inhibitor (RTI) was seen in 25 (39.7%) patients, to nonnucleoside RTIs in 5 (8%) patients, and to protease inhibitors in 4 (6%) patients. The high prevalence we observed in this study may limit in future the effectiveness of ARV programs in the Côte d'Ivoire.
authors.affiliation: Projet RETRO-CI, Abidjan, Côte d'Ivoire; Division of AIDS, STD, TB Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, USA.
authors.forename: C
authors.initials: C
authors.lastname: Adjé
authors.forename: R
authors.initials: R
authors.lastname: Cheingsong
authors.forename: T H
authors.initials: TH
authors.lastname: Roels
authors.forename: C
authors.initials: C
authors.lastname: Maurice
authors.forename: G
authors.initials: G
authors.lastname: Djomand
authors.forename: W
authors.initials: W
authors.lastname: Verbiest
authors.forename: K
authors.initials: K
authors.lastname: Hertogs
authors.forename: B
authors.initials: B
authors.lastname: Larder
authors.forename: B
authors.initials: B
authors.lastname: Monga
authors.forename: M
authors.initials: M
authors.lastname: Peeters
authors.forename: S
authors.initials: S
authors.lastname: Eholie
authors.forename: E
authors.initials: E
authors.lastname: Bissagene
authors.forename: M
authors.initials: M
authors.lastname: Coulibaly
authors.forename: R
authors.initials: R
authors.lastname: Respess
authors.forename: S Z
authors.initials: SZ
authors.lastname: Wiktor
authors.forename: T
authors.initials: T
authors.lastname: Chorba
authors.forename: J N
authors.initials: JN
authors.lastname: Nkengasong
mesh_terms: D019380:Anti-HIV Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007560:Cote d'Ivoire / Q000453:epidemiology; D004352:Drug Resistance, Microbial / Q000235:genetics; D018432:Drug Resistance, Multiple / Q000235:genetics; D004359:Drug Therapy, Combination; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology* / Q000821:virology*; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D009154:Mutation; D010641:Phenotype; D010802:Phylogeny; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D017422:Sequence Analysis, DNA
chemical_list: D019380:Anti-HIV Agents; D018894:Reverse Transcriptase Inhibitors