The HIV-1 protease substitution K55R: a protease-inhibitor-associated substitution involved in restoring viral replication

J Antimicrob Chemother. 2008 Apr;61(4):786-91. doi: 10.1093/jac/dkm545. Epub 2008 Feb 4.

Abstract

Objectives: The identification and in vitro characterization of novel protease mutations strongly associated with known protease resistance mutations.

Methods: The association between pairs of protease amino acid substitutions was identified using a database of protease sequences derived from protease inhibitor-experienced patients (n = 803). In vitro characterization included drug susceptibility and viral replication studies performed on recombinant viruses harbouring site-directed mutations.

Results: The K55R mutation, which is not a natural polymorphism, was identified to be strongly associated with protease mutations M46I/L and to a lesser extent L24I, I54V and V82A/T/S/F. In vitro characterization of the K55R substitution indicated a primary role for this substitution in increasing replicative capacity in the presence of specific protease mutations.

Conclusions: The K55R mutation is a secondary drug resistance mutation that can improve viral replication capacity in the presence of other primary protease mutations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Substitution*
  • Drug Resistance, Viral / genetics*
  • HIV Infections / virology
  • HIV Protease / genetics*
  • HIV Protease / physiology
  • HIV Protease Inhibitors / pharmacology*
  • HIV-1 / drug effects
  • HIV-1 / genetics*
  • HIV-1 / physiology*
  • Humans
  • Microbial Sensitivity Tests
  • Mutagenesis, Site-Directed
  • Mutation, Missense
  • Virus Replication*

Substances

  • HIV Protease Inhibitors
  • HIV Protease
  • p16 protease, Human immunodeficiency virus 1