Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1

J Clin Invest. 1998 Oct 15;102(8):1540-50. doi: 10.1172/JCI4151.


Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms. We demonstrate that () macrophages exposed to bacterial cell wall components such as lipopolysaccharide (LPS) (Gram-negative rods), lipoteichoic acid (Gram-positive cocci), and lipoarabinomannan (Mycobacteria) become highly susceptible to T cell (T)-tropic HIV-1 (which otherwise poorly replicate in macrophages) and variably susceptible to macrophage (M)-tropic HIV-1; () LPS-stimulated macrophages secrete a number of soluble factors (i.e., chemokines, interferon, and proinflammatory cytokines) that variably affect HIV infection of macrophages, depending on the virus phenotype in question; and () LPS-stimulated macrophages express CCR5 (a major coreceptor for M-tropic HIV-1) at lower levels and CXCR4 (a major coreceptor for T-tropic HIV-1) at higher levels compared with unstimulated macrophages. We hypothesize that a more favorable environment for T-tropic HIV-1 and a less favorable or even unfavorable environment for M-tropic HIV-1 secondary to exposure of macrophages to those bacterial products may accerelate a transition from M- to T-tropic viral phenotype, which is indicative of disease progression.

MeSH terms

  • Cell Wall / chemistry
  • Chemokines / metabolism
  • Culture Media, Conditioned
  • Cytokines / metabolism
  • Gram-Positive Cocci / immunology
  • HIV-1 / classification
  • HIV-1 / pathogenicity*
  • Interferons / metabolism
  • Lipopolysaccharide Receptors / metabolism
  • Lipopolysaccharides / pharmacology*
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / virology*
  • Mycobacterium / immunology
  • Protein Kinase C / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, CCR5 / biosynthesis
  • Receptors, CXCR4 / biosynthesis
  • Signal Transduction
  • T-Lymphocytes / virology
  • Teichoic Acids / pharmacology
  • Virus Replication


  • Chemokines
  • Culture Media, Conditioned
  • Cytokines
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • Receptors, CCR5
  • Receptors, CXCR4
  • Teichoic Acids
  • lipoarabinomannan
  • lipoteichoic acid
  • Interferons
  • Protein-Tyrosine Kinases
  • Protein Kinase C