AN INTEGRAL MEMBRANE-PROTEIN (LMP2) BLOCKS REACTIVATION OF EPSTEIN-BARR-VIRUS FROM LATENCY FOLLOWING SURFACE-IMMUNOGLOBULIN CROSS-LINKING
AN INTEGRAL MEMBRANE-PROTEIN (LMP2) BLOCKS REACTIVATION OF EPSTEIN-BARR-VIRUS FROM LATENCY FOLLOWING SURFACE-IMMUNOGLOBULIN CROSS-LINKING
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DOI：
10.1073/pnas.91.2.772
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发表时间：
1994-01-18
影响因子：
11.1
通讯作者：
LONGNECKER, R
中科院分区：
文献类型：
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作者：
MILLER, CL;LEE, JH;LONGNECKER, R
用EB病毒（EBV）野生型或特异性突变重组体转化的潜伏感染原代B淋巴细胞评价潜伏膜蛋白2（LMP 2）在EBV感染中的作用。LMP 2无效突变重组EBV感染的细胞与正常B淋巴细胞在表面免疫球蛋白交联后细胞内游离钙的快速增加相似。这些细胞也变得更允许裂解性EBV复制。与此形成鲜明对比的是，野生型对照感染细胞的细胞内游离钙或EBV复制的过氧化物酶几乎没有增加或没有增加。通过用离子载体提高细胞内游离钙水平和用佛波醇12-肉豆蔻酸酯13-乙酸酯激活蛋白激酶C，可以绕过表达野生型LMP 2的细胞中的表面免疫球蛋白交联诱导的阻断。LMP 2A而不是LMP 2B介导了这种对钙动员的影响。遗传和生物化学数据与这些效应一致，这些效应是由于LMP 2A N-末端胞质结构域与B淋巴细胞src家族酪氨酸激酶的相互作用。
The role of latent membrane protein 2 (LMP2) in Epstein-Barr virus (EBV) infection was evaluated by using latently infected primary B lymphocytes that had been growth transformed by wild-type or specifically mutated EBV recombinants. LMP2 null mutant recombinant EBV-infected cells were similar to normal B lymphocytes in their rapid increase in intracellular free calcium after surface immunoglobulin crosslinking. These cells also became more permissive for lytic EBV replication. In sharp contrast, wild-type control infected cells had little or no increase in intracellular free calcium or in permissivity For EBV replication. The block to surface immunoglobulin crosslinking induced permissivity in cells expressing wild-type LMP2 could be bypassed by raising intracellular free calcium levels with an ionophore and by activating protein kinase C with phorbol 12-myristate 13-acetate. LMP2A, not LMP2B, mediates this effect on calcium mobilization. Genetic and biochemical data are consistent with these effects being due to the interaction of the LMP2A N-terminal cytoplasmic domain with B lymphocyte src family tyrosine kinases.