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      CD4-independent infection by HIV-2 is mediated by fusin/CXCR4.

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          Abstract

          Several members of the chemokine receptor family have been shown to function in association with CD4 to permit HIV-1 entry and infection. However, the mechanism by which these molecules serve as CD4-associated cofactors is unclear. In the present report, we show that one member of this family, termed Fusin/ CXCR4, is able to function as an alternative receptor for some isolates of HIV-2 in the absence of CD4. This conclusion is supported by the finding that (1) CD4-independent infection by these viruses is inhibited by an anti-Fusin monoclonal antibody, (2) Fusin expression renders human and nonhuman CD4-negative cell lines sensitive to HIV-2-induced syncytium induction and/or infection, and (3) Fusin is selectively down-regulated from the cell surface following HIV-2 infection. The finding that one chemokine receptor can function as a primary viral receptor strongly suggests that the HIV envelope glycoprotein contains a binding site for these proteins and that differences in the affinity and/or the availability of this site can extend the host range of these viruses to include a number of CD4-negative cell types.

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          Author and article information

          Journal
          Cell
          Cell
          0092-8674
          0092-8674
          Nov 15 1996
          : 87
          : 4
          Affiliations
          [1 ] Hematology-Oncology Division, University of Pennsylvania, Philadelphia 19104, USA.
          Article
          S0092-8674(00)81393-8
          8929542

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