Potent inhibition of HIV-1 infectivity in macrophages and lymphocytes by a novel CCR5 antagonist

Science. 1997 Apr 11;276(5310):276-9. doi: 10.1126/science.276.5310.276.

Abstract

The chemokine receptors CXCR4 and CCR5 have recently been shown to act as coreceptors, in concert with CD4, for human immunodeficiency virus-type 1 (HIV-1) infection. RANTES and other chemokines that interact with CCR5 and block infection of peripheral blood mononuclear cell cultures inhibit infection of primary macrophages inefficiently at best. If used to treat HIV-1-infected individuals, these chemokines could fail to influence HIV replication in nonlymphocyte compartments while promoting unwanted inflammatory side effects. A derivative of RANTES that was created by chemical modification of the amino terminus, aminooxypentane (AOP)-RANTES, did not induce chemotaxis and was a subnanomolar antagonist of CCR5 function in monocytes. It potently inhibited infection of diverse cell types (including macrophages and lymphocytes) by nonsyncytium-inducing, macrophage-tropic HIV-1 strains. Thus, activation of cells by chemokines is not a prerequisite for the inhibition of viral uptake and replication. Chemokine receptor antagonists like AOP-RANTES that achieve full receptor occupancy at nanomolar concentrations are strong candidates for the therapy of HIV-1-infected individuals.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding, Competitive
  • CD4 Antigens / metabolism
  • Cats
  • Cell Line
  • Cells, Cultured
  • Chemokine CCL4
  • Chemokine CCL5 / metabolism
  • Chemokine CCL5 / pharmacology
  • Chemotaxis, Leukocyte
  • HIV-1 / drug effects*
  • HIV-1 / physiology
  • HeLa Cells
  • Humans
  • Macrophage Inflammatory Proteins / metabolism
  • Macrophages / drug effects
  • Macrophages / virology*
  • Receptors, CCR5
  • Receptors, Chemokine*
  • Receptors, Cytokine / antagonists & inhibitors*
  • Receptors, Cytokine / metabolism
  • Receptors, HIV / antagonists & inhibitors*
  • Receptors, HIV / metabolism
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / virology*
  • Virus Replication / drug effects

Substances

  • CD4 Antigens
  • Chemokine CCL4
  • Chemokine CCL5
  • Macrophage Inflammatory Proteins
  • Receptors, CCR5
  • Receptors, Chemokine
  • Receptors, Cytokine
  • Receptors, HIV