title: Prevalence and patterns of HIV transmitted drug resistance in Guatemala.
abstract: OBJECTIVE
  To assess human immunodeficiency virus (HIV) diversity and the prevalence of transmitted drug resistance (TDR) in Guatemala.
  
  
  METHODS
  One hundred forty-five antiretroviral treatment-naïve patients referred to the Roosevelt Hospital in Guatemala City were enrolled from October 2010 to March 2011. Plasma HIV pol sequences were obtained and TDR was assessed with the Stanford algorithm and the World Health Organization (WHO) TDR surveillance mutation list.
  
  
  RESULTS
  HIV subtype B was highly prevalent in Guatemala (96.6%, 140/145), and a 2.8% (4/145) prevalence of BF1 recombinants and 0.7% (1/145) prevalence of subtype C viruses were found. TDR prevalence for the study period was 8.3% (12/145) with the Stanford database algorithm (score > 15) and the WHO TDR surveillance mutation list. Most TDR cases were associated with non-nucleoside reverse transcriptase inhibitors (NNRTIs) (83.3%, 10/12); a low prevalence of nucleoside reverse transcriptase inhibitors and protease inhibitors was observed in the cohort (< 1% for both families). Low selection of antiretroviral drug resistance mutations was found, except for NNRTI-associated mutations. Major NNRTI mutations such as K101E, K103N, and E138K showed higher frequencies than expected in ART-naïve populations. Higher literacy was associated with a greater risk of TDR (odds ratio 4.14, P = 0.0264).
  
  
  CONCLUSIONS
  This study represents one of the first efforts to describe HIV diversity and TDR prevalence and trends in Guatemala. TDR prevalence in Guatemala was at the intermediate level. Most TDR cases were associated with NNRTIs. Further and continuous TDR surveillance is necessary to gain more indepth knowledge about TDR spread and trends in Guatemala and to optimize treatment outcomes in the country.
authors.affiliation: Centro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico.
authors.forename: Santiago
authors.initials: S
authors.lastname: Avila-Ríos
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Mejía-Villatoro
authors.forename: Claudia
authors.initials: C
authors.lastname: García-Morales
authors.forename: Maribel
authors.initials: M
authors.lastname: Soto-Nava
authors.forename: Ingrid
authors.initials: I
authors.lastname: Escobar
authors.forename: Ricardo
authors.initials: R
authors.lastname: Mendizabal
authors.forename: Amalia
authors.initials: A
authors.lastname: Girón
authors.forename: Leticia
authors.initials: L
authors.lastname: García
authors.forename: Gustavo
authors.initials: G
authors.lastname: Reyes-Terán
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology* / Q000627:therapeutic use; D024882:Drug Resistance, Viral / Q000235:genetics; D004522:Educational Status; D005260:Female; D015751:Genes, pol; D005838:Genotype; D006166:Guatemala / Q000453:epidemiology; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology / Q000821:virology; D017320:HIV Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D008297:Male; D017720:Molecular Epidemiology; D020125:Mutation, Missense; D017354:Point Mutation; D011159:Population Surveillance; D015995:Prevalence; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use
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