Non-active site changes elicit broad-based cross-resistance of the HIV-1 protease to inhibitors

J Biol Chem. 1999 Aug 20;274(34):23699-701. doi: 10.1074/jbc.274.34.23699.

Abstract

Three high level, cross-resistant variants of the HIV-1 protease have been analyzed for their ability to bind four protease inhibitors approved by the Food and Drug Administration (saquinavir, ritonavir, indinavir, and nelfinavir) as AIDS therapeutics. The loss in binding energy (DeltaDeltaG(b)) going from the wild-type enzyme to mutant enzymes ranges from 2.5 to 4.4 kcal/mol, 40-65% of which is attributed to amino acid substitutions away from the active site of the protease and not in direct contact with the inhibitor. The data suggest that non-active site changes are collectively a major contributor toward engendering resistance against the protease inhibitor and cannot be ignored when considering cross-resistance issues of drugs against the HIV-1 protease.

MeSH terms

  • Binding Sites
  • Drug Resistance
  • HIV Protease / chemistry
  • HIV Protease / drug effects*
  • HIV Protease Inhibitors / pharmacology*
  • Indinavir / pharmacology
  • Protein Conformation
  • Structure-Activity Relationship
  • Thermodynamics

Substances

  • HIV Protease Inhibitors
  • Indinavir
  • HIV Protease