Abstract
The beta-chemokines MIP-1alpha, MIP-1beta and RANTES inhibit infection of CD4+ T cells by primary, non-syncytium-inducing (NSI) HIV-1 strains at the virus entry stage, and also block env-mediated cell-cell membrane fusion. CD4+ T cells from some HIV-1-exposed uninfected individuals cannot fuse with NSI HIV-1 strains and secrete high levels of beta-chemokines. Expression of the beta-chemokine receptor CC-CKR-5 in CD4+, non-permissive human and non-human cells renders them susceptible to infection by NSI strains, and allows env-mediated membrane fusion. CC-CKR-5 is a second receptor for NSI primary viruses.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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CD4-Positive T-Lymphocytes / virology*
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Cell Line
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Cells, Cultured
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Chemokine CCL3
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Chemokine CCL4
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Chemokine CCL5 / metabolism
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Chemokine CCL5 / pharmacology
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DNA Primers
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Gene Products, env / metabolism
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HIV Infections / virology
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HIV-1 / pathogenicity
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HIV-1 / physiology*
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HeLa Cells
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Humans
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Macrophage Inflammatory Proteins
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Macrophages / virology
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Membrane Fusion
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Molecular Sequence Data
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Monokines / metabolism
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Monokines / pharmacology
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Receptors, CCR5
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Receptors, Cytokine / genetics
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Receptors, Cytokine / metabolism*
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Receptors, Virus / metabolism*
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Recombinant Proteins / metabolism
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Virus Replication
Substances
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Chemokine CCL3
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Chemokine CCL4
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Chemokine CCL5
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DNA Primers
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Gene Products, env
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Macrophage Inflammatory Proteins
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Monokines
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Receptors, CCR5
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Receptors, Cytokine
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Receptors, Virus
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Recombinant Proteins