Virus-associated host CD62L increases attachment of human immunodeficiency virus type 1 to endothelial cells and enhances trans infection of CD4+ T lymphocytes.
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.
Thibault
Sandra
S
Research Center in Infectious Diseases, CHUL Research Center, and Faculty of Medicine, Laval University, Quebec, Canada.
Tardif
Mélanie R
MR
Research Center in Infectious Diseases, CHUL Research Center, and Faculty of Medicine, Laval University, Quebec, Canada.
Gilbert
Caroline
C
Research Center in Infectious Diseases, CHUL Research Center, and Faculty of Medicine, Laval University, Quebec, Canada.
Tremblay
Michel J
MJ
Research Center in Infectious Diseases, CHUL Research Center, and Faculty of Medicine, Laval University, Quebec, Canada.
D015496:CD4-Positive T-Lymphocytes / Q000821:virology*; D002448:Cell Adhesion; D004730:Endothelium, Vascular / Q000276:immunology / Q000821:virology*; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D019041:L-Selectin / Q000502:physiology*; D014471:Umbilical Veins; D014771:Virion / Q000276:immunology
D019041:L-Selectin