Khélifa R, Menezes J
J Virol. 1982 May;42(2):402-10. doi: 10.1128/JVI.42.2.402-410.1982.
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.
为研究爱泼斯坦 - 巴尔病毒（EBV）侵入靶细胞的某些方面，检测了刀豆蛋白A（ConA）和各种糖类对病毒感染性以及细胞对EBV感染易感性的影响。发现用ConA处理靶细胞、EBV或EBV - 细胞复合物可抑制病毒抗原表达。进行了多项对照实验，包括用α - d - 甲基甘露糖苷洗脱ConA、用胰蛋白酶处理去除细胞表面未融合的EBV颗粒以及在感染后不同时间添加ConA，以确定ConA对EBV感染作用的位点。ConA似乎具有双重作用：（i）它抑制EBV与病毒受体的结合，（ii）它在胰蛋白酶敏感阶段阻断受体结合病毒进入靶细胞，从而表明ConA阻止了病毒包膜与靶细胞膜的融合。已知高蔗糖浓度（0.25 M）可抑制细胞膜运动，也发现在胰蛋白酶敏感阶段阻断EBV侵入，因此提示细胞膜运动及潜在活动（或两者）与病毒包膜融合有关。较低浓度的各种单糖（0.12 M）不影响EBV感染。在不影响EBV感染性和靶细胞易感性的ConA处理条件下，ConA能够介导病毒与EBV受体阴性细胞系结合，但这些细胞中未表达病毒抗原。这些观察结果强化了这样一种观点，即EBV仅附着于淋巴细胞不足以导致感染。根据目前及先前发表的数据，我们推测存在一种特定的细胞机制，使EBV能够侵入靶（B）淋巴细胞。
