Abstract
Epstein-Barr virus, the causative agent of mononucleosis and several human cancers, infects cells via complement receptor type 2 (CR2). Expression of this receptor is restricted to B lymphocytes, some epithelial cells and immature thymocytes; expression of CR2-like proteins has been also found on T cells. In the present report, we identified the presence, on the membrane of Li7A cells, of a novel EBV receptor distinct from CR2 capable of triggering fusion with EBV virions with more rapid kinetics than that found with lymphoblastoid cells (Raji).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carcinoma, Hepatocellular / microbiology*
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Cell Membrane / metabolism
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Complement C3d / pharmacology
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Hematopoietic Stem Cells / microbiology
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Herpesvirus 4, Human / growth & development*
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Humans
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Kinetics
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Liver Neoplasms / microbiology*
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Lymphocytes / microbiology
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Membrane Fusion* / drug effects
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Receptors, Complement / analysis
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Receptors, Complement 3d
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Receptors, Virus / metabolism*
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Tumor Cells, Cultured
Substances
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Receptors, Complement
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Receptors, Complement 3d
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Receptors, Virus
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Complement C3d