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Expression and function of CCR5 and CXCR4 on human Langerhans cells and macrophages: implications for HIV primary

M Zaitseva1, A Blauvelt, S Lee

  • 1Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.

Nature Medicine
|December 13, 1997
PubMed

Insights

Human immunodeficiency virus type 1 (HIV-1) primarily infects macrophages via M-tropic strains. This study reveals that Langerhans cells express CCR5, facilitating M-tropic HIV-1 fusion, while macrophages show functional CCR5, explaining selective HIV-1 transmission.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human immunodeficiency virus type 1 (HIV-1) transmission is often restricted to macrophage (Mphi)-tropic strains.
  • Langerhans cells (LCs) in mucosal epithelium and submucosal macrophages are potential initial targets for HIV-1.

Purpose of the Study:

  • To investigate the correlation between HIV-1 co-receptor expression and function on LCs and macrophages and the restricted transmission of HIV-1.
  • To determine the role of CXCR4 and CCR5 in HIV-1 entry into these cells.

Main Methods:

  • Freshly isolated epidermal LCs and macrophages were analyzed for surface and intracellular expression of HIV-1 co-receptors (CXCR4 and CCR5) using specific antibodies.
  • Fusion assays were performed using HIV-1 envelopes (M-tropic and T-tropic) to assess co-receptor functionality.

Main Results:

  • Epidermal LCs expressed CCR5 but not CXCR4 on their surface, fusing with M-tropic but not T-tropic HIV-1 envelopes.
  • Intracellular CXCR4 was detected in fresh LCs and transported to the surface during in vitro culture.
  • Macrophages expressed both CCR5 and CXCR4, but only CCR5 demonstrated functionality in fusion assays.

Conclusions:

  • The expression profile of CCR5 on LCs and macrophages contributes to the selective transmission of M-tropic HIV-1 variants.
  • Functional CCR5 on macrophages and its presence on LCs may explain the observed patterns of HIV-1 transmission and resistance associated with CCR5 deletion.

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