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HIV-1 protease mutation 82M contributes to phenotypic resistance to protease inhibitors in subtype G

Ana Carolina Palma1, Kris Covens, Joke Snoeck

  • 1Clinical and Epidemiological Virology, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium. acmpalma@gmail.com

The Journal of Antimicrobial Chemotherapy
|February 15, 2012
PubMed
Abstract

Insights

The HIV-1 protease mutation 82M impacts protease inhibitor susceptibility, not viral replication. This finding supports including 82M in drug resistance interpretation systems for better HIV treatment.

Area of Science:

  • Virology
  • Drug Resistance Studies
  • Molecular Biology

Background:

  • Human Immunodeficiency Virus type 1 (HIV-1) protease (PR) is a key target for antiretroviral therapy.
  • Mutations in the PR gene can lead to resistance against available protease inhibitors (PIs).
  • Understanding the impact of specific mutations on viral fitness and drug susceptibility is crucial for optimizing treatment strategies.

Purpose of the Study:

  • To assess the in vitro effect of the HIV-1 PR 82M mutation on viral replication capacity.
  • To quantify the susceptibility of HIV-1 with the 82M mutation to eight clinically available PIs.
  • To determine if the 82M mutation confers drug resistance or affects viral fitness.

Main Methods:

  • Site-directed mutagenesis was used to introduce the 82M substitution into wild-type subtype B and G HIV-1 strains.
  • The 82M mutation was also reverted to wild-type in a therapy-failing strain.
  • Recombinant viruses were evaluated for replication capacity and susceptibility to PIs in vitro.

Main Results:

  • The single 82M mutation did not confer drug resistance in wild-type subtype B or G backgrounds.
  • Reverting 82M to wild-type (82I) in a therapy-failing subtype G isolate significantly increased susceptibility to indinavir and lopinavir.
  • The 82M mutation slightly decreased viral replication capacity in both subtype B and G backgrounds.

Conclusions:

  • The 82M mutation impacts PI susceptibility, independent of its effect on replication capacity.
  • The observed impact on PI susceptibility suggests 82M should be included in drug resistance interpretation systems.
  • The absence of 82M as a common polymorphism supports its significance as a resistance-associated mutation.

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