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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1997-1-2
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pubmed:abstractText |
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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pubmed:language |
eng
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pubmed:journal |
|
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pubmed:citationSubset |
IM
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|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
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|
pubmed:month |
Nov
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|
pubmed:issn |
0092-8674
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pubmed:author |
pubmed-author:AhujaMM,
pubmed-author:ChoiWW,
pubmed-author:ClaphamP RPR,
pubmed-author:DomsR WRW,
pubmed-author:EndresM JMJ,
pubmed-author:HoxieJ AJA,
pubmed-author:LandauN RNR,
pubmed-author:MarshMM,
pubmed-author:McKnightAA,
pubmed-author:PowerC ACA,
pubmed-author:Stoebenau-HaggartyBB,
pubmed-author:SutterwalaS SSS,
pubmed-author:ThomasJ FJF,
pubmed-author:TurnerJ DJD,
pubmed-author:VanceP JPJ,
pubmed-author:WellsT NTN
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pubmed:issnType |
Print
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|
pubmed:day |
15
|
|
pubmed:volume |
87
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|
pubmed:owner |
NLM
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|
pubmed:authorsComplete |
Y
|
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pubmed:pagination |
745-56
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8929542-Animals,
pubmed-meshheading:8929542-Antibodies, Monoclonal,
pubmed-meshheading:8929542-Antigens, CD4,
pubmed-meshheading:8929542-B-Lymphocytes,
pubmed-meshheading:8929542-Base Sequence,
pubmed-meshheading:8929542-CHO Cells,
pubmed-meshheading:8929542-Cell Fusion,
pubmed-meshheading:8929542-Cricetinae,
pubmed-meshheading:8929542-Down-Regulation,
pubmed-meshheading:8929542-Genetic Variation,
pubmed-meshheading:8929542-HIV-2,
pubmed-meshheading:8929542-Humans,
pubmed-meshheading:8929542-Lymphocytes,
pubmed-meshheading:8929542-Membrane Proteins,
pubmed-meshheading:8929542-Molecular Sequence Data,
pubmed-meshheading:8929542-Quail,
pubmed-meshheading:8929542-Receptors, CXCR4,
pubmed-meshheading:8929542-Receptors, HIV,
pubmed-meshheading:8929542-Recombinant Proteins,
pubmed-meshheading:8929542-T-Lymphocytes
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pubmed:year |
1996
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|
pubmed:articleTitle |
CD4-independent infection by HIV-2 is mediated by fusin/CXCR4.
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pubmed:affiliation |
Hematology-Oncology Division, University of Pennsylvania, Philadelphia 19104, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
