title: Characterization of drug resistance in antiretroviral-treated patients infected with HIV-1 CRF02_AG and AGK subtypes in Mali and Burkina Faso.
abstract: BACKGROUND
  In a multicentred cohort of patients on antiretroviral therapy (ART) in Burkina Faso and Mali, we analysed the prevalence of HIV drug resistance mutations in patients failing a modified directly observed therapy (mDOT) protocol.
  
  
  METHODS
  Patients on ART >6 months and with viral load (VL) >500 copies/ml were enrolled in a mDOT protocol. Genotypic resistance testing was performed on pre- and post-mDOT plasma samples of patients who still had VL >500 copies/ml after mDOT.
  
  
  RESULTS
  Eight hundred and one patients from seven sites participated in the study. One hundred and thirteen patients (14.1%) had VL >500 copies/ml. Most patients were treated with lamivudine along with zidovudine or stavudine and efavirenz or nevirapine. Genotypes were available for 46 patients. The predominant HIV-1 subtypes were CRFO2_AG in 26 (56.5%) and AGK/K/AK in 12 (26.1%) patients. The prevalence of drug resistance mutations by class were as follows for nucleoside reverse transcriptase inhibitors: 1841/V (82.6%), 215Y/F (32.6%), 219E/Q (19.6%), 70R (19.6%), 67N (21.7%), 41L (15.2%) and 151M(2.2%). For non-nucleoside reverse transcriptase inhibitors the prevalence was: 103N (50%) and 181C/I (19.6%). Phylogenetic analysis showed that, although the genetic distances were small among isolates, there was no clustering of a particular subtype in a specific region and that the high prevalence of AGK subtype in our drug-resistant population was not due to a circulating resistant strain.
  
  
  CONCLUSIONS
  Although CRFO2_AG is the dominant clade in the Burkina Faso/Mali region, isolates with subtype K reverse transcriptase were frequent in our cohort. Drug resistance mutation pathways in subtype K reverse transcriptase need to be further evaluated in a larger cohort of non-B HIV-infected individuals.
authors.affiliation: Département de Microbiologie et Immunologie, Université de Montréal, Montréal, Canada.
authors.forename: Mohamed
authors.initials: M
authors.lastname: Sylla
authors.forename: Annie
authors.initials: A
authors.lastname: Chamberland
authors.forename: Catherine
authors.initials: C
authors.lastname: Boileau
authors.forename: Hamar A
authors.initials: HA
authors.lastname: Traoré
authors.forename: Souleyman
authors.initials: S
authors.lastname: Ag-Aboubacrine
authors.forename: Mamadou
authors.initials: M
authors.lastname: Cissé
authors.forename: Samual
authors.initials: S
authors.lastname: Koala
authors.forename: Joseph
authors.initials: J
authors.lastname: Drabo
authors.forename: Ismael
authors.initials: I
authors.lastname: Diallo
authors.forename: Pascal
authors.initials: P
authors.lastname: Niamba
authors.forename: Daniel
authors.initials: D
authors.lastname: Tremblay-Sher
authors.forename: Nimâ
authors.initials: N
authors.lastname: Machouf
authors.forename: Sélim
authors.initials: S
authors.lastname: Rashed
authors.forename: David C
authors.initials: DC
authors.lastname: Nickle
authors.forename: Vinh-Kim
authors.initials: VK
authors.lastname: Nguyen
authors.forename: Cécile L
authors.initials: CL
authors.lastname: Tremblay
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D002050:Burkina Faso / Q000453:epidemiology; D024882:Drug Resistance, Viral; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000453:epidemiology / Q000821:virology; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D008297:Male; D008302:Mali / Q000453:epidemiology; D009154:Mutation; D010802:Phylogeny
chemical_list: D019380:Anti-HIV Agents