HIV-1 Entry Into CD4+ Cells Is Mediated by the Chemokine Receptor CC-CKR-5

Nature. 1996 Jun 20;381(6584):667-73. doi: 10.1038/381667a0.

Abstract

The beta-chemokines MIP-1alpha, MIP-1beta and RANTES inhibit infection of CD4+ T cells by primary, non-syncytium-inducing (NSI) HIV-1 strains at the virus entry stage, and also block env-mediated cell-cell membrane fusion. CD4+ T cells from some HIV-1-exposed uninfected individuals cannot fuse with NSI HIV-1 strains and secrete high levels of beta-chemokines. Expression of the beta-chemokine receptor CC-CKR-5 in CD4+, non-permissive human and non-human cells renders them susceptible to infection by NSI strains, and allows env-mediated membrane fusion. CC-CKR-5 is a second receptor for NSI primary viruses.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence
  • CD4-Positive T-Lymphocytes / virology*
  • Cell Line
  • Cells, Cultured
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5 / metabolism
  • Chemokine CCL5 / pharmacology
  • DNA Primers
  • Gene Products, env / metabolism
  • HIV Infections / virology
  • HIV-1 / pathogenicity
  • HIV-1 / physiology*
  • HeLa Cells
  • Humans
  • Macrophage Inflammatory Proteins
  • Macrophages / virology
  • Membrane Fusion
  • Molecular Sequence Data
  • Monokines / metabolism
  • Monokines / pharmacology
  • Receptors, CCR5
  • Receptors, Cytokine / genetics
  • Receptors, Cytokine / metabolism*
  • Receptors, Virus / metabolism*
  • Recombinant Proteins / metabolism
  • Virus Replication

Substances

  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • DNA Primers
  • Gene Products, env
  • Macrophage Inflammatory Proteins
  • Monokines
  • Receptors, CCR5
  • Receptors, Cytokine
  • Receptors, Virus
  • Recombinant Proteins