Apricitabine does not select additional drug resistance mutations in tissue culture in human immunodeficiency virus type 1 variants containing K65R, M184V, or M184V plus thymidine analogue mutations

Antimicrob Agents Chemother. 2009 Apr;53(4):1683-5. doi: 10.1128/AAC.01168-08. Epub 2009 Feb 17.

Abstract

Human immunodeficiency virus type 1 containing the reverse transcriptase mutation M184V or K65R or mutations M41L, M184V, and T215Y did not accumulate additional resistance mutations in the reverse transcriptase when increasing amounts of apricitabine drug pressure were applied. The original mutations were maintained by the presence of apricitabine but were lost when cultured without drug pressure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-HIV Agents / pharmacology*
  • Deoxycytidine / analogs & derivatives*
  • Deoxycytidine / pharmacology
  • Drug Resistance, Viral / genetics
  • HIV Reverse Transcriptase / genetics*
  • HIV-1 / genetics*
  • Mutation*
  • Reverse Transcriptase Inhibitors / pharmacology*
  • Stavudine / pharmacology
  • Zidovudine / pharmacology

Substances

  • Anti-HIV Agents
  • Reverse Transcriptase Inhibitors
  • Deoxycytidine
  • Zidovudine
  • Stavudine
  • reverse transcriptase, Human immunodeficiency virus 1
  • HIV Reverse Transcriptase
  • apricitabine