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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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

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.[1]

References

  1. CD4-independent infection by HIV-2 is mediated by fusin/CXCR4. Endres, M.J., Clapham, P.R., Marsh, M., Ahuja, M., Turner, J.D., McKnight, A., Thomas, J.F., Stoebenau-Haggarty, B., Choe, S., Vance, P.J., Wells, T.N., Power, C.A., Sutterwala, S.S., Doms, R.W., Landau, N.R., Hoxie, J.A. Cell (1996) [Pubmed]
 
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