title: Genotypic human immunodeficiency virus type 1 drug resistance in highly active antiretroviral therapy-treated children in Abidjan, Côte d'Ivoire.
abstract: OBJECTIVE
  To estimate the frequency of human immunodeficiency virus type 1 (HIV-1) displaying genotypic drug resistance in highly active antiretroviral therapy (HAART)-treated children in Abidjan.
  
  
  METHODS
  Among the 269 HIV-1-infected children enrolled in the ANRS 1278 prospective observational cohort between October 2000 and September 2003, 115 [median age, 6.35 years (range, 1.2-15)] required treatment and received HAART for at least 6 months. Treatment consisted of 2 nucleoside analogue reverse transcriptase inhibitors associated with nelfinavir (70.5%) or efavirenz (29.5%). Plasma HIV-1 RNA and CD4+ T cell counts were determined at baseline and every 6 months thereafter. Genotypic resistance tests were performed in cases of virologic failure (viral load >or=3 log10 copies/mL) after at least 6 months of HAART.
  
  
  RESULTS
  After a median of 10.2 months of HAART, 66% (76 of 115) of children were in virologic success. Most of these children were infected with CRF02 strains. Twenty-seven viruses displayed resistance to at least 1 antiretroviral drug (27 of 38, 71%). Thirteen, 9 and 5 children had viruses with resistance to 1, 2 or 3 of the drugs included in their regimen, respectively. Resistance to lamivudine and/or to non-nucleoside analogue reverse transcriptase inhibitors was frequent among the 38 children in virologic failure. The 90M, 46L, 88S or 54V mutations were found in 11 (38%) of the 29 children taking nelfinavir. The overall frequency of viruses showing genotypic resistance to at least 1 antiretroviral drug was 23% (27 of 115) among the treated children.
  
  
  CONCLUSIONS
  These results are similar to what is generally observed in industrialized countries. Despite these encouraging results, efforts are needed to maximize the long-term efficiency of treatment and to minimize the risk of emergence of drug resistance in treated children.
authors.affiliation: Service de Virologie-EA 3620 Université René Descartes, CHU Necker-Enfants Malades, Paris, France. marie-laure.chaix@nck.ap-hop-paris.fr
authors.forename: Marie-Laure
authors.initials: ML
authors.lastname: Chaix
authors.forename: François
authors.initials: F
authors.lastname: Rouet
authors.forename: Kouakou Alain
authors.initials: KA
authors.lastname: Kouakoussui
authors.forename: Rockiath
authors.initials: R
authors.lastname: Laguide
authors.forename: Patricia
authors.initials: P
authors.lastname: Fassinou
authors.forename: Crepin
authors.initials: C
authors.lastname: Montcho
authors.forename: Stéphane
authors.initials: S
authors.lastname: Blanche
authors.forename: Christine
authors.initials: C
authors.lastname: Rouzioux
authors.forename: Philippe
authors.initials: P
authors.lastname: Msellati
mesh_terms: D000293:Adolescent; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D007560:Cote d'Ivoire / Q000453:epidemiology; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D007223:Infant; D008297:Male; D009154:Mutation; D010802:Phylogeny; D012367:RNA, Viral / Q000097:blood; D019562:Viral Load
chemical_list: D012367:RNA, Viral; D054303:HIV Reverse Transcriptase; D016333:HIV Protease