EBV lytic infection enhances transformation of B-lymphocytes infected with EBV in the presence of T-lymphocytes
EBV lytic infection enhances transformation of B-lymphocytes infected with EBV in the presence of T-lymphocytes
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DOI：
10.1002/jmv.23208
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发表时间：
2012-03-01
影响因子：
12.7
通讯作者：
Takada, Kenzo
中科院分区：
文献类型：
--
作者：
Katsumura, Koichi Ricardo;Maruo, Seiji;Takada, Kenzo
EB病毒（EBV）感染后在B淋巴细胞中建立终身潜伏期。尽管在免疫活性个体中EBV保持静止状态，但在免疫缺陷个体中，例如患有AIDS或移植受体的那些，被EBV感染的B淋巴细胞增殖以引起淋巴增生性疾病。类似地，在体外，EBV在不存在细胞毒性T淋巴细胞的情况下将人B淋巴细胞转化为无限生长的淋巴母细胞样细胞系（LCL）。尽管LCL携带作为附加体的整个EBV基因组，但在大多数细胞中，病毒保持在表达一部分EBV基因的潜伏状态，并且裂解性感染自发地发生，但仅在一小部分细胞中发生。在这里，我们报告，裂解感染有助于EB病毒诱导的淋巴细胞增殖的旁分泌机制。EBV立即早期蛋白BZLF 1诱导IL-13，从而促进EBV转化的B淋巴细胞在T淋巴细胞存在下的增殖。这些数据表明，裂解基因产物可能有助于病毒诱导的肿瘤发生的旁分泌机制。医学病毒学杂志84：504510，2012。(C)2011 Wiley Periodicals，Inc.
EpsteinBarr virus (EBV) establishes lifelong latency in B-lymphocytes following infection. Although in immune-competent individuals EBV remains in a quiescent state, in immunodeficient individuals, such as those with AIDS or transplant recipients, B-lymphocytes infected with EBV proliferate to give rise to lymphoproliferative diseases. Similarly, in vitro, EBV transforms human B-lymphocytes into indefinitely growing lymphoblastoid cell lines (LCLs) in the absence of cytotoxic T-lymphocytes. Although LCLs harbor the entire EBV genome as an episome, in most cells the virus remains in a latent state expressing a fraction of EBV genes, and lytic infection occurs spontaneously but only in a small percentage of cells. Here, we report that lytic infection contributes to EBV-induced lymphoproliferation by a paracrine mechanism. An EBV immediate-early protein, BZLF1, induces IL-13, thus facilitating the proliferation of EBV-transformed B-lymphocytes in the presence of T-lymphocytes. These data suggest that lytic gene products could contribute to virus-induced oncogenesis by a paracrine mechanism. J. Med. Virol. 84:504510, 2012. (C) 2011 Wiley Periodicals, Inc.