CD4-independent infection by HIV-2 is mediated by fusin/CXCR4 - PubMed (original) (raw)

Comparative Study

. 1996 Nov 15;87(4):745-56.

doi: 10.1016/s0092-8674(00)81393-8.

P R Clapham, M Marsh, M Ahuja, J D Turner, A McKnight, J F Thomas, B Stoebenau-Haggarty, S Choe, P J Vance, T N Wells, C A Power, S S Sutterwala, R W Doms, N R Landau, J A Hoxie

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Free article

Comparative Study

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

M J Endres et al. Cell. 1996.

Free article

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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