Abstract
Human immunodeficiency virus-type 1 (HIV-1) entry requires fusion cofactors on the CD4+ target cell. Fusin, a heterotrimeric GTP-binding protein (G protein)-coupled receptor, serves as a cofactor for T cell line-tropic isolates. The chemokines RANTES, MIP-1alpha, and MIP-1beta, which suppress infection by macrophage-tropic isolates, selectively inhibited cell fusion mediated by the corresponding envelope glycoproteins (Envs). Recombinant CC CKR5, a G protein-coupled receptor for these chemokines, rendered CD4-expressing nonhuman cells fusion-competent preferentially with macrophage-tropic Envs. CC CKR5 messenger RNA was detected selectively in cell types susceptible to macrophage-tropic isolates. CC CKR5 is thus a fusion cofactor for macrophage-tropic HIV-1 strains.
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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3T3 Cells
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Animals
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CD4 Antigens / physiology
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Cell Fusion
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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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Chemokines / metabolism*
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Chemokines / pharmacology
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Gene Products, env / physiology
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Giant Cells / metabolism
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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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Mice
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Monokines / metabolism
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Monokines / pharmacology
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Receptors, CCR5
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Receptors, Cytokine / physiology*
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Receptors, HIV / physiology*
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Recombinant Proteins / pharmacology
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T-Lymphocytes / virology
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Tumor Cells, Cultured
Substances
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CD4 Antigens
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Chemokine CCL3
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Chemokine CCL4
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Chemokine CCL5
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Chemokines
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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, HIV
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Recombinant Proteins