[Epidemiology of genotypic resistance of HIV-1 in Valencia. A 4-year study]

Rev Esp Quimioter. 2007 Sep;20(3):346-53.
[Article in Spanish]

Abstract

HIV resistance to antiretroviral drugs was studied in 348 samples taken from patients at the Molecular Biology Unit of the Microbiology Department of the Hospital La Fe, from January 2003 to July 2007. Once the viral load in plasma was determined, resistance was detected using complete gene sequencing for protease up to position 3464 of the HIV-1 reverse transcriptase gene. The results were analyzed using the Omiga 1.2 (Oxford Molecular Group) and HIV db Genotypic Resistance Interpretation Algorithm Version 4.3.0 (Stanford University) programs. The drugs least affected by the presence of mutations leading to resistance were the protease inhibitors darunavir, tripanavir and lopinavir (sensitivity >80%), the nucleoside reverse transcriptase inhibitors tenofovir and lamivudine (sensitivity >90%) and the non-nucleoside reverse transcriptase inhibitor TMC125 (sensitivity >80%).

Publication types

  • English Abstract

MeSH terms

  • Algorithms
  • Amino Acid Substitution
  • Anti-HIV Agents / pharmacology*
  • Anti-HIV Agents / therapeutic use
  • Drug Resistance, Multiple, Viral / genetics*
  • Follow-Up Studies
  • Genotype
  • HIV Infections / drug therapy
  • HIV Infections / epidemiology
  • HIV Infections / microbiology*
  • HIV Protease / genetics
  • HIV Protease Inhibitors / pharmacology
  • HIV Reverse Transcriptase / genetics
  • HIV-1 / drug effects*
  • HIV-1 / isolation & purification
  • Humans
  • Mutation, Missense
  • Point Mutation
  • RNA, Viral / genetics
  • Reverse Transcriptase Inhibitors / pharmacology
  • Sequence Analysis, RNA
  • Spain / epidemiology
  • Viral Load

Substances

  • Anti-HIV Agents
  • HIV Protease Inhibitors
  • RNA, Viral
  • Reverse Transcriptase Inhibitors
  • reverse transcriptase, Human immunodeficiency virus 1
  • HIV Reverse Transcriptase
  • HIV Protease
  • p16 protease, Human immunodeficiency virus 1