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

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 and Dana Gabuzda
Additional contact information
Jianglin He: Harvard Medical School
Hyeryun Choe: Harvard Medical School
Asa Ohagen: Harvard Medical School
Xiaoyu Yang: Harvard Medical School
Wolfgang Hofmann: Harvard Medical School
Joseph Sodroski: Harvard Medical School

Nature, 1997, vol. 385, issue 6617, 645-649

Abstract: 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.

Date: 1997
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DOI: 10.1038/385645a0

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