title: Adherence to protease inhibitors, HIV-1 viral load, and development of drug resistance in an indigent population.
abstract: OBJECTIVE
  To examine the relationship between adherence, viral suppression and antiretroviral resistance in HIV-infected homeless and marginally housed people on protease inhibitor (PI) therapy.
  
  
  METHODS
  A cross-sectional analysis of subjects in an observational prospective cohort systematically sampled from free meal lines, homeless shelters and low-income, single-room occupancy (SRO) hotels.
  
  
  METHODS
  Thirty-four HIV-infected people with a median of 12 months of PI therapy.
  
  
  RESULTS
  Adherence measured by periodic unannounced pill counts, electronic medication monitoring, and self-report; HIV RNA viral load; and HIV-1 genotypic changes associated with drug resistance.
  
  
  RESULTS
  Median adherence was 89, 73, and 67% by self-report, pill count, and electronic medication monitor, respectively. Thirty-eight per cent of the population had over 90% adherence by pill count. Depending on the measure, adherence explained 36-65% of the variation in concurrent HIV RNA levels. The three adherence measures were closely related. Of 20 genotyped patients who received a new reverse transcriptase inhibitor (RTI) when starting a PI, three had primary protease gene substitutions. Of 12 genotyped patients who received a PI without a new RTI, six had primary protease gene substitutions (P < 0.03).
  
  
  CONCLUSIONS
  A substantial proportion of homeless and marginally housed individuals had good adherence to PI therapy. A strong relationship was found between independent methods of measuring adherence and concurrent viral suppression. PI resistance was more closely related to the failure to change RTI when starting a PI than to the level of adherence.
authors.affiliation: Epidemiology and Prevention Interventions Center, Division of Infectious Diseases, San Francisco General Hospital, University of California San Francisco, 94110, USA. db@epi-center.ucsf.edu
authors.forename: D R
authors.initials: DR
authors.lastname: Bangsberg
authors.forename: F M
authors.initials: FM
authors.lastname: Hecht
authors.forename: E D
authors.initials: ED
authors.lastname: Charlebois
authors.forename: A R
authors.initials: AR
authors.lastname: Zolopa
authors.forename: M
authors.initials: M
authors.lastname: Holodniy
authors.forename: L
authors.initials: L
authors.lastname: Sheiner
authors.forename: J D
authors.initials: JD
authors.lastname: Bamberger
authors.forename: M A
authors.initials: MA
authors.lastname: Chesney
authors.forename: A
authors.initials: A
authors.lastname: Moss
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000008:administration & dosage / Q000627:therapeutic use; D015331:Cohort Studies; D004352:Drug Resistance, Microbial / Q000235:genetics*; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D017320:HIV Protease Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D015497:HIV-1 / Q000235:genetics / Q000302:isolation & purification; D006703:Ill-Housed Persons; D006801:Humans; D008297:Male; D008489:Medical Indigency; D015999:Multivariate Analysis; D010349:Patient Compliance; D018894:Reverse Transcriptase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors