title: Primary drug resistance in antiretroviral-naïve injection drug users.
abstract: OBJECTIVE
  We evaluated the prevalence of primary HIV drug resistance in a population of 128 injection drug users (48 female) prior to initiating antiretroviral therapy.
  
  
  METHODS
  Genotypic and phenotypic profiles were obtained retrospectively for the period June 1996 to February 2007. Genotypic drug resistance was defined as the presence of a major mutation (IAS-USA table, 2007 revision), adding revertants at reverse transcriptase (RT) codon 215. Phenotypic drug resistance was defined as the fold change associated with >or=80% loss of the wild type virologic response due to viral resistance based on virtual phenotype analysis.
  
  
  RESULTS
  Genotypic drug resistance was uncommon, and was only identified in six (4.7%) cases, all in the RT gene (L100I, K103N, Y181C, M184V, Y188L, and T215D). There were no cases of multi-class or protease inhibitor (PI) resistance. However, polymorphisms in the protease and RT genes were extremely common. Phenotypic drug resistance was also identified in six (4.7%) patients, four in the RT gene (in patients with mutations K103N, Y181C, M184V and Y188L) and two the protease gene (in two patients with minor PI mutations). In addition, 25 (19.5%) of the patients had reduced susceptibility to PIs, defined as resistance>20% but <80% of the wild type virologic response, with no primary PI mutations detected in all these patients.
  
  
  CONCLUSIONS
  The prevalence of primary HIV drug resistance was low in this population of injection drug users.
authors.affiliation: Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, 2176 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.
authors.forename: Harout K
authors.initials: HK
authors.lastname: Tossonian
authors.forename: Jesse D
authors.initials: JD
authors.lastname: Raffa
authors.forename: Jason
authors.initials: J
authors.lastname: Grebely
authors.forename: Mark
authors.initials: M
authors.lastname: Viljoen
authors.forename: Annabel
authors.initials: A
authors.lastname: Mead
authors.forename: Milan
authors.initials: M
authors.lastname: Khara
authors.forename: Mark
authors.initials: M
authors.lastname: McLean
authors.forename: Ashok
authors.initials: A
authors.lastname: Krishnamurthy
authors.forename: Stanley
authors.initials: S
authors.lastname: DeVlaming
authors.forename: Brian
authors.initials: B
authors.lastname: Conway
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002170:Canada; D024882:Drug Resistance, Viral / Q000235:genetics; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy* / Q000821:virology; D016333:HIV Protease / Q000235:genetics; D017320:HIV Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests / Q000379:methods; D008875:Middle Aged; D009154:Mutation; D010641:Phenotype; D015995:Prevalence; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D015819:Substance Abuse, Intravenous / Q000150:complications*
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; C514824:reverse transcriptase, Human immunodeficiency virus 1; D054303:HIV Reverse Transcriptase; D016333:HIV Protease