Development and significance of resistance to protease inhibitors in HIV-1-infected adults under triple-drug therapy in clinical practice

J Med Virol. 2002 Feb;66(2):143-50. doi: 10.1002/jmv.2123.

Abstract

Development of drug resistance is considered a major cause for failure of antiretroviral therapy in human immunodeficiency virus type 1 (HIV-1)-infected patients adherent to treatment. However, the rate of emergence and the significance of HIV-1 drug resistance in clinical practice have been not investigated thoroughly. Selection of HIV-1 variants that are genotypically resistant to protease inhibitors was studied in all the patients (n = 169) who completed at least 18 months of treatment with a protease inhibitor plus two nucleoside reverse transcriptase inhibitors at two urban Italian hospitals. HIV-1 carrying primary protease inhibitor resistance mutations was detected in 70 (41.4%) patients. The estimated proportion of patients developing genotypic resistance to protease inhibitors at 12 and 24 months was 18.3% (95% CI, 12.5-24.2%) and 33.9% (95% CI, 26.4-41.5%), respectively. Independent predictors of development of resistance to protease inhibitors were higher HIV-1 RNA levels at the nadir (P < 0.0001) and inclusion of ritonavir or saquinavir versus indinavir in the starting regimen (P = 0.0313). Resistance to protease inhibitors was strongly associated with a lower response to treatment, as shown by HIV-1 RNA load (P = 0.0001) and CD4 cell counts (P = 0.005). However, a linear increase in CD4 cell counts was maintained up to the end of follow-up even in the protease inhibitor-resistant population. Resistance to protease inhibitors develops in a relevant proportion of patients under long-term triple-drug therapy in clinical practice and is associated with virological treatment failure and limitation of CD4 cell increase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-HIV Agents / pharmacology
  • Anti-HIV Agents / therapeutic use
  • CD4 Lymphocyte Count
  • Drug Resistance, Viral / genetics*
  • Drug Therapy, Combination
  • HIV Infections / drug therapy*
  • HIV Infections / immunology
  • HIV Infections / virology
  • HIV Protease / genetics*
  • HIV Protease Inhibitors / pharmacology*
  • HIV Protease Inhibitors / therapeutic use
  • HIV-1 / drug effects*
  • HIV-1 / genetics
  • HIV-1 / physiology
  • Humans
  • RNA, Viral / blood
  • Reverse Transcriptase Inhibitors / pharmacology
  • Reverse Transcriptase Inhibitors / therapeutic use
  • Treatment Outcome

Substances

  • Anti-HIV Agents
  • HIV Protease Inhibitors
  • RNA, Viral
  • Reverse Transcriptase Inhibitors
  • HIV Protease