Antiretroviral drug resistance in HIV-2: three amino acid changes are sufficient for classwide nucleoside analogue resistance

Robert A. Smith, Donovan J. Anderson, Crystal L. Pyrak, Bradley D. Preston, Geoffrey S. Gottlieb

Research output: Contribution to journalArticlepeer-review

54 Scopus citations

Abstract

Genotypic surveys suggest that human immunodeficiency virus type 1 (HIV-1) and HIV-2 evolve different sets of mutations in response to nucleoside reverse-transcriptase inhibitors (NRTIs). We used site-directed mutagenesis, culturebased phenotyping, and cell-free assays to determine the resistance profiles conferred by specific amino acid replacements in HIV-2 reverse transcriptase. Although thymidine analogue mutations had no effect on zidovudine sensitivity, the addition of Q151M together with K65R or M184V was sufficient for high-level resistance to both lamivudine and zidovudine in HIV-2, and the combination of K65R, Q151M, and M184V conferred classwide NRTI resistance. These data suggest that current NRTI-based regimens are suboptimal for treating HIV-2 infection.

Original languageEnglish (US)
Pages (from-to)1323-1326
Number of pages4
JournalJournal of Infectious Diseases
Volume199
Issue number9
DOIs
StatePublished - May 1 2009
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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