title: [Rate of genotypic mutations and resistance to antiretroviral drugs in a general hospital].
abstract: OBJECTIVE
  The objective is to describe the resistance mutation rate in protease and reverse transcriptase genes and sensitivity to different antiretrovirals in our environment.
  
  
  METHODS
  We performed an observational descriptive study in which we examined the samples provided at the clinical immunology laboratory between April 2004 and April 2009. We analysed both the resistance tests and the sensitivity to different drugs in patients with therapeutic failure using trugene hiv01 genotyping kits(®).
  
  
  RESULTS
  We registered samples from 242 patients, 61 of which had no detectable resistance. The most prevalent mutations according to drug families were: for nucleoside analog reverse transcriptase inhibitors T215A/C/D/F/L/N/S/Y (24.10%), M184G/I/V/W (14.66%), M41J/L/R/T/W (11.24%) and K219E/G/H/N/R/T/W (10.24%). The highest levels of resistance corresponded to stavudine and lamivudine/emtricitabine, and tenofovir produced the least resistance in our environment. The non-analogues were K103N/R (23.98%), V179D/E/I/M/T (10.82%), A98E/G/S (10.53%) y K101E/P/Q/R (9.06%). Nevirapine presented greater resistance than efavirenz. Protease inhibitors were L10F/I/V (15.95%), M36I/L (13.81%), A71I/T/V (13.10%) and 154L/S/V (7.38%). The combination darunavir/ritonavir combination was that which presented the least resistance, and tipranavir/ritonavir and lopinavir/ritonavir the most resistance.
  
  
  CONCLUSIONS
  Antiretroviral resistance and sensitivity to retroviral treatment in our environment was similar to results from other studies in Spain, but differed in the high level of resistance to lamivudine/emtricitabine and lopinavir/ritonavir.
authors.affiliation: Servicio de Farmacia Hospitalaria, Complejo Hospitalario de Cáceres, Cáceres, España. lcfernandezlison@hotmail.com
authors.forename: L C
authors.initials: LC
authors.lastname: Fernández Lisón
authors.forename: L M
authors.initials: LM
authors.lastname: Fernández Pereira
authors.forename: S
authors.initials: S
authors.lastname: Romero Chala
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology*; D024921:Drug Resistance, Multiple, Viral / Q000235:genetics; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy; D016333:HIV Protease / Q000235:genetics*; D017320:HIV Protease Inhibitors / Q000494:pharmacology*; D054303:HIV Reverse Transcriptase / Q000037:antagonists & inhibitors / Q000235:genetics*; D015497:HIV-1 / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D006769:Hospitals, General / Q000706:statistics & numerical data; D006801:Humans; D008297:Male; D055118:Medication Adherence; D008875:Middle Aged; D009154:Mutation; D017354:Point Mutation; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology*; D013030:Spain; D019562:Viral Load
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; C514803:p16 protease, Human immunodeficiency virus 1