Abstract
Chemokine receptors serve as portals of entry for certain intracellular pathogens, most notably human immunodeficiency virus (HIV). Myxoma virus is a member of the poxvirus family that induces a lethal systemic disease in rabbits, but no poxvirus receptor has ever been defined. Rodent fibroblasts (3T3) that cannot be infected with myxoma virus could be made fully permissive for myxoma virus infection by expression of any one of several human chemokine receptors, including CCR1, CCR5, and CXCR4. Conversely, infection of 3T3-CCR5 cells can be inhibited by RANTES, anti-CCR5 polyclonal antibody, or herbimycin A but not by monoclonal antibodies that block HIV-1 infection or by pertussis toxin. These findings suggest that poxviruses, like HIV, are able to use chemokine receptors to infect specific cell subtypes, notably migratory leukocytes, but that their mechanisms of receptor interactions are distinct.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3 Cells
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Animals
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Antibodies / immunology
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Benzoquinones
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Cell Line
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Chemokine CCL5 / pharmacology
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Chlorocebus aethiops
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Gene Expression
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Humans
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Lactams, Macrocyclic
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Mice
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Myxoma virus / genetics
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Myxoma virus / metabolism*
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Pertussis Toxin
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Quinones / pharmacology
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Receptors, CCR1
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Receptors, CCR5 / immunology
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Receptors, CCR5 / metabolism
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Receptors, CXCR4 / metabolism
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Receptors, Chemokine / metabolism*
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Receptors, Virus / metabolism*
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Rifabutin / analogs & derivatives
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Signal Transduction
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Tumor Cells, Cultured
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Virulence Factors, Bordetella / pharmacology
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beta-Galactosidase / biosynthesis
Substances
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Antibodies
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Benzoquinones
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CCR1 protein, human
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Ccr1 protein, mouse
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Chemokine CCL5
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Lactams, Macrocyclic
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Quinones
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Receptors, CCR1
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Receptors, CCR5
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Receptors, CXCR4
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Receptors, Chemokine
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Receptors, Virus
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Virulence Factors, Bordetella
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Rifabutin
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herbimycin
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Pertussis Toxin
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beta-Galactosidase