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Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
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Identification of a major co-receptor for primary isolates of HIV-1

H Deng1, R Liu, W Ellmeier

  • 1Skirball Institute for BioMolecular Medicine, New York University Medical Center, 10016, USA.

Nature
|June 20, 1996
PubMed

Insights

Researchers discovered that CC-chemokine receptor 5 (CC-CKR-5) is essential for macrophage-tropic HIV-1 entry into host cells. This finding is crucial as fusin, previously identified, does not facilitate entry of these key pathogenic viral strains.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • HIV-1 entry into target cells necessitates CD4 and host cell cofactors.
  • Fusin, a recently identified cofactor, supports infection by T-cell line-adapted HIV-1.
  • Fusin does not mediate entry of macrophage-tropic HIV-1, the primary in vivo pathogenic strains.

Purpose of the Study:

  • To identify the principal cofactor for entry of macrophage-tropic HIV-1 strains.
  • To elucidate the molecular mechanisms of HIV-1 viral entry.

Main Methods:

  • The study likely involved experiments assessing viral entry mediated by different cofactors.
  • Analysis of envelope glycoproteins from primary macrophage-tropic HIV-1 strains was performed.

Main Results:

  • Fusin is not the cofactor for macrophage-tropic HIV-1 entry.
  • CC-chemokine receptor 5 (CC-CKR-5) serves as the principal cofactor for entry mediated by macrophage-tropic HIV-1 envelope glycoproteins.
  • CC-CKR-5 is a known receptor for beta-chemokines RANTES, MIP-1alpha, and MIP-1beta.

Conclusions:

  • CC-CKR-5 is a critical determinant of cellular tropism for pathogenic HIV-1 strains.
  • Understanding these cofactors is vital for developing effective anti-HIV therapies targeting viral entry.

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