Abstract
We examined the ability of chemokine receptors and related G protein-coupled receptors to facilitate infection by primary, clinical HIV-1 isolates. CCR5, when expressed along with CD4, the HIV-1 receptor, allowed cell lines resistant to most primary HIV-1 isolates to be infected. CCR3 facilitated infection by a more restricted subset of primary viruses, and binding of the CCR3 ligand, eotaxin, inhibited infection by these isolates. Utilization of CCR3 and CCR5 on the target cell depended upon the sequence of the third variable (V3) region of the HIV-1 gp120 exterior envelope glycoprotein. The ability of various members of the chemokine receptor family to support the early stages of HIV-1 infection helps to explain viral tropism and beta-chemokine inhibition of primary HIV-1 isolates.
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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Acquired Immunodeficiency Syndrome / virology*
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Animals
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CD4 Antigens / physiology
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Cell Fusion / physiology
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Chemokine CCL11
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Chemokines / physiology
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Chemokines, CC*
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Cytokines / pharmacology
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Dogs
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Glycoproteins / physiology
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HIV-1 / drug effects
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HIV-1 / physiology*
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HeLa Cells / chemistry
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HeLa Cells / physiology
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HeLa Cells / virology
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Humans
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Macrophages / chemistry
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Macrophages / virology
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Receptors, CCR3
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Receptors, CCR5
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Receptors, Chemokine*
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Receptors, Cytokine / drug effects
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Receptors, Cytokine / physiology*
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Receptors, HIV / physiology
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T-Lymphocytes / chemistry
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T-Lymphocytes / virology
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Thymus Gland / cytology
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Viral Envelope Proteins / physiology
Substances
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CCL11 protein, human
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CCR3 protein, human
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CD4 Antigens
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Chemokine CCL11
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Chemokines
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Chemokines, CC
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Cytokines
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Glycoproteins
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Receptors, CCR3
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Receptors, CCR5
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Receptors, Chemokine
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Receptors, Cytokine
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Receptors, HIV
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Viral Envelope Proteins