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Co-receptors for HIV-1 entry

J P Moore1, A Trkola, T Dragic

  • 1The Aaron Diamond AIDS Research Center, The Rockefeller University, 455 First Avenue, New York, NY 10021, USA. jmoore@adarc.org

Current Opinion in Immunology
|August 1, 1997
PubMed
Summary

Human immunodeficiency virus type 1 (HIV-1) requires specific co-receptors, CXCR4 and CCR5, for cell entry. These co-receptors, targeted by chemokines, are essential for viral fusion and infection.

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • HIV-1 infection initiates through viral fusion with host target cells at the plasma membrane.
  • CD4 is the primary cellular receptor for HIV-1, but it is insufficient alone for viral entry.
  • The identification of co-receptors in 1996 was a critical breakthrough in understanding HIV-1 cell entry.

Purpose of the Study:

  • To elucidate the role of co-receptors in HIV-1 cell entry.
  • To identify the specific co-receptors utilized by different HIV-1 strains.
  • To understand the mechanism by which natural ligands affect co-receptor function.

Main Methods:

  • Identification of seven-transmembrane-spanning receptors involved in viral fusion.
  • Characterization of co-receptor usage by T-tropic and M-tropic HIV-1 strains.
  • Investigation of the inhibitory effects of alpha- and beta-chemokine ligands on co-receptor function.

Main Results:

  • Co-receptors, specifically CXCR4 and CCR5, were identified as essential for HIV-1 entry.
  • CXCR4 mediates entry for T-tropic HIV-1 strains.
  • CCR5 is the principal co-receptor for M-tropic HIV-1 strains.
  • Natural chemokine ligands inhibit the co-receptor functions of CXCR4 and CCR5.

Conclusions:

  • CXCR4 and CCR5 are crucial co-receptors for HIV-1 cell entry, dictating tropism.
  • The interaction of HIV-1 with CD4 and these co-receptors is essential for viral fusion.
  • Chemokine binding to co-receptors modulates HIV-1 infectivity, offering potential therapeutic targets.

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