Abstract
Occasional EBV infection of human NK cells may lead to malignant diseases such as naso-pharyngeal NK lymphoma although NK cells do not express CD21, the primary receptor for EBV. Here we show that during early EBV infection in patients, NK cells attacked EBV-infected autologous B cells. In vitro, NK cells activated by conjugation to CD21(+) B-EBV cell targets transiently acquired a weak CD21(+) phenotype by synaptic transfer of few receptor molecules onto their own membrane. In the presence of viral particles, these ectopic receptors allowed EBV binding to the novel NK cell host. Hence, trans-synaptic acquisition of viral receptor from target cells might constitute an unsuspected mode of infection for otherwise unreachable lymphoid hosts.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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B-Lymphocyte Subsets / immunology
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B-Lymphocyte Subsets / pathology
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B-Lymphocyte Subsets / virology
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Binding Sites / immunology
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Cell Communication / immunology*
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Cell Membrane / immunology
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Cell Membrane / metabolism
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Cell Membrane / virology
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Cell Survival / immunology
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Cells, Cultured
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Coculture Techniques
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Cytotoxicity Tests, Immunologic
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Herpesvirus 4, Human / immunology*
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Herpesvirus 4, Human / isolation & purification
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Herpesvirus 4, Human / metabolism
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Humans
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Immunophenotyping
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Infectious Mononucleosis / immunology
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Infectious Mononucleosis / pathology
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Infectious Mononucleosis / virology
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K562 Cells
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Killer Cells, Natural / immunology*
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Killer Cells, Natural / metabolism
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Killer Cells, Natural / virology*
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Lymph Nodes / immunology
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Lymph Nodes / pathology
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Lymph Nodes / virology
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Receptors, Complement 3d / biosynthesis
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Receptors, Complement 3d / metabolism
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Receptors, Virus / metabolism*
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Tumor Cells, Cultured
Substances
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Receptors, Complement 3d
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Receptors, Virus