Virus-associated host CD62L increases attachment of human immunodeficiency virus type 1 to endothelial cells and enhances trans infection of CD4+ T lymphocytes

J Gen Virol. 2007 Sep;88(Pt 9):2568-2573. doi: 10.1099/vir.0.83032-0.

Abstract

Previous studies have identified several host-derived cell-surface proteins incorporated within emerging human immunodeficiency virus type 1 (HIV-1) particles. Some of these molecules play a role in different steps of the virus life cycle and are often advantageous for the virus. We report here that the leukocyte L-selectin (also called CD62L) remains functional when inserted within the envelope of HIV-1. Indeed, we demonstrate that adsorption of virions to endothelial cells is enhanced upon acquisition of host-derived CD62L. The more important binding of CD62L-bearing HIV-1 particles resulted in a more efficient virus transmission to CD4(+) T lymphocytes. Capture and eventual transfer of such CD62L-bearing virions by the endothelium could play a role in the pathogenesis of HIV-1 infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / virology*
  • Cell Adhesion
  • Endothelium, Vascular / immunology
  • Endothelium, Vascular / virology*
  • HIV Infections / immunology*
  • HIV-1 / immunology
  • HIV-1 / pathogenicity
  • HIV-1 / physiology*
  • Humans
  • L-Selectin / physiology*
  • Umbilical Veins
  • Virion / immunology

Substances

  • L-Selectin