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CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia

Author

Listed:
  • Jianglin He

    (Harvard Medical School
    Harvard Medical School)

  • Youzhi Chen
  • Michael Farzan
  • Hyeryun Choe

    (Harvard Medical School
    Harvard Medical School)

  • Asa Ohagen

    (Harvard Medical School
    Harvard Medical School)

  • Suzanne Gartner
  • Jorge Busciglio
  • Xiaoyu Yang

    (Harvard Medical School
    Harvard Medical School)

  • Wolfgang Hofmann

    (Harvard Medical School
    Harvard Medical School)

  • Walter Newman
  • Charles R. Mackay
  • Joseph Sodroski

    (Harvard Medical School
    Harvard Medical School)

  • Dana Gabuzda

Abstract

Several members of the chemokine receptor family are used together with CD4 for HIV-1 entry into target cells1–6. T cell line-tropic (T-tropic) HIV-1 viruses use the chemokine receptor CXCR4 as a co-receptor1, whereas macrophage-tropic (M-tropic) primary viruses use CCR5 (refs 2–6). Individuals with defective CCR5 alleles exhibit resistance to HIV-1 infection7,8, suggesting that CCR5 has an important role in vivo in HIV-1 replication. A subset of primary viruses can use CCR3 as well as CCR5 as a co-receptor5,6, but the in vivo contribution of CCR3 to HIV-1 infection and pathogenesis is unknown. HIV-1 infects the central nervous system (CNS) and causes the dementia associated with AIDS9. Here we report that the major target cells for HIV-1 infection in the CNS, the microglia9–11, express both CCR3 and CCR5. The CCR3 ligand, eotaxin, and an anti-CCR3 antibody inhibited HIV-1 infection of microglia, as did MIP-1β, which is a CCR5 ligand. Our results suggest that both CCR3 and CCR5 promote efficient infection of the CNS by HIV-1.

Suggested Citation

  • Jianglin He & Youzhi Chen & Michael Farzan & Hyeryun Choe & Asa Ohagen & Suzanne Gartner & Jorge Busciglio & Xiaoyu Yang & Wolfgang Hofmann & Walter Newman & Charles R. Mackay & Joseph Sodroski & Dana, 1997. "CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia," Nature, Nature, vol. 385(6617), pages 645-649, February.
    • Handle: RePEc:nat:nature:v:385:y:1997:i:6617:d:10.1038_385645a0
    DOI: 10.1038/385645a0
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