The magnitude of HIV-1 resistance to the CCR5 antagonist maraviroc may impart a differential alteration in HIV-1 tropism for macrophages and T-cell subsets

Virology. 2013 Jul 20;442(1):51-8. doi: 10.1016/j.virol.2013.03.026. Epub 2013 Apr 17.

Abstract

Human immunodeficiency virus type 1 (HIV-1) resistance to CCR5 antagonists, including maraviroc (MVC), results from alterations in the HIV-1 envelope glycoproteins (Env) enabling recognition of antagonist-bound CCR5. Here, we characterized tropism alterations for CD4+ T-cell subsets and macrophages by Envs from two subjects who developed MVC resistance in vivo, which displayed either relatively efficient or inefficient recognition of MVC-bound CCR5. We show that MVC-resistant Env with efficient recognition of drug-bound CCR5 displays a tropism shift for CD4+ T-cell subsets associated with increased infection of central memory T-cells and reduced infection of effector memory and transitional memory T-cells, and no change in macrophage infectivity. In contrast, MVC-resistant Env with inefficient recognition of drug-bound CCR5 displays no change in tropism for CD4+ T-cell subsets, but exhibits a significant reduction in macrophage infectivity. The pattern of HIV-1 tropism alterations for susceptible cells may therefore be variable in subjects with MVC resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CCR5 Receptor Antagonists*
  • CD4-Positive T-Lymphocytes / virology*
  • Cell Line
  • Cyclohexanes / pharmacology*
  • Drug Resistance, Viral*
  • HIV Envelope Protein gp120 / metabolism
  • HIV Fusion Inhibitors / pharmacology*
  • HIV-1 / drug effects*
  • HIV-1 / pathogenicity*
  • Humans
  • Macrophages / virology*
  • Maraviroc
  • T-Lymphocyte Subsets / virology
  • Triazoles / pharmacology*

Substances

  • CCR5 Receptor Antagonists
  • Cyclohexanes
  • HIV Envelope Protein gp120
  • HIV Fusion Inhibitors
  • Triazoles
  • Maraviroc