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, Dana Gabuzda

Research output: Contribution to journalArticlepeer-review

777 Scopus citations


Several members of the chemokine receptor family are used together with CD4 for HIV-1 entry into target cells. T cell line-tropic (T-tropic) HIV-1 viruses use the chemokine receptor CXCR4 as a co-receptor, whereas macrophage-tropic (M-tropic) primary viruses use CCR5. Individuals with defective CCR5 alleles exhibit resistance to HIV-1 infection, 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-receptor, 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 AIDS. Here we report that the major target cells for HIV-1 infection in the CNS, the microglia, express both CCR3 and CCRS. 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.

Original languageEnglish (US)
Pages (from-to)645-647
Number of pages3
Issue number6617
StatePublished - Feb 13 1997

ASJC Scopus subject areas

  • General


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