C-C chemokines released by lipopolysaccharide (LPS)-stimulated human macrophages suppress HIV-1 infection in both macrophages and T cells

J Exp Med. 1997 Mar 3;185(5):805-16. doi: 10.1084/jem.185.5.805.

Abstract

Human immunodeficiency virus-1 (HIV-1) expression in monocyte-derived macrophages (MDM) infected in vitro is known to be inhibited by lipopolysaccharide (LPS). However, the mechanisms are incompletely understood. We show here that HIV-1 suppression is mediated by soluble factors released by MDM stimulated with physiologically significant concentrations of LPS. LPS-conditioned supernatants from MDM inhibited HIV-1 replication in both MDM and T cells. Depletion of C-C chemokines (RANTES, MIP-1 alpha, and MIP-1 beta) neutralized the ability of LPS-conditioned supernatants to inhibit HIV-1 replication in MDM. A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS. Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages. Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Chemokine CCL4
  • Chemokine CCL5 / metabolism
  • Chemokine CCL5 / pharmacology
  • Chemokines / metabolism
  • Chemokines / pharmacology*
  • DNA, Viral / analysis
  • Enzyme-Linked Immunosorbent Assay
  • HIV-1 / drug effects
  • HIV-1 / growth & development*
  • Humans
  • Interleukin-6 / pharmacology
  • Lipopolysaccharide Receptors / biosynthesis
  • Lipopolysaccharides / pharmacology*
  • Macrophage Inflammatory Proteins / metabolism
  • Macrophage Inflammatory Proteins / pharmacology
  • Macrophages / drug effects
  • Macrophages / virology*
  • Polymerase Chain Reaction
  • Receptors, CCR5
  • Receptors, Cytokine / biosynthesis
  • Receptors, HIV / biosynthesis
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / virology*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Up-Regulation
  • Virus Replication / drug effects

Substances

  • Chemokine CCL4
  • Chemokine CCL5
  • Chemokines
  • DNA, Viral
  • Interleukin-6
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • Macrophage Inflammatory Proteins
  • Receptors, CCR5
  • Receptors, Cytokine
  • Receptors, HIV
  • Tumor Necrosis Factor-alpha