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).
Early steps in fusion between Epstein Barr Virus (EBV) and a human hepatoma cell line (Li7A)
Lisi A;Lanzilli G;Grimaldi S
1993
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).File in questo prodotto:
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