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pubmed:abstractText |
To study some aspects of Epstein-Barr virus (EBV) penetration into target cells, the effect of concanavalin A (ConA) and various saccharides on virus infectivity and cell susceptibility to EBV infection was examined. ConA treatment of the target cells, EBV, or EBV-cell complexes was found to inhibit virus antigen expression. Several control experiments with alpha-d-methyl-mannoside elution of ConA, removal of nonfused EBV particles from the cell surface by trypsin treatment, and addition of ConA at different times postinfection were performed to define the site of ConA action on EBV infection. ConA appeared to have a dual action: (i) it inhibited EBV binding to virus receptors, and (ii) it blocked the penetration of receptor-bound virus into target cells at a trypsin-sensitive stage, thus indicating that ConA prevented the fusion of viral envelope with the target cell membrane. A high sucrose concentration (0.25 M), known to inhibit cell membrane movements, was also found to block EBV penetration at a trypsinsensitive stage, thus suggesting the implication of cell membrane movements and underlying activities (or both) in viral envelope fusion. Lower concentrations of various monosaccharides (0.12 M) did not influence EBV infection. Under conditions of ConA treatment that did not influence EBV infectivity and target cells susceptibility, ConA was able to mediate virus binding to EBV receptornegative cell lines, but no virus antigens were expressed in these cells. These observations reinforced the idea that the mere attachment of EBV to lymphoid cells is not sufficient to lead to infection. In light of the present and previously published data, we postulate the existence of a specific cellular mechanism that allows the penetration of EBV into the target (B) lymphocyte.
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