Merchant M, Swart R, Katzman R B, Ikeda M, Ikeda A, Longnecker R, Dykstra M L, Pierce S K
Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Int Rev Immunol. 2001;20(6):805-35. doi: 10.3109/08830180109045591.
Epstein-Barr Virus (EBV) infects B-lymphocytes circulating through the oral epithelium and establishes a lifelong latent infection in a subset of mature-memory B cells. In these latently infected B cells, EBV exhibits limited gene expression with the latent membrane protein 2A (LMP2A) being the most consistently detected transcript. This persistent expression, coupled with many studies ofthe function of LMP2A in vitro and invivo, indicates that LMP2A is functioning to control some aspect of viral latency. Establishment and maintenance of viral latency requires exquisite manipulation of normal B cell signaling and function. LMP2A is capable of blocking normal B cell signal transduction in vitro, suggesting that LMP2A may act to regulate lytic activation from latency in vivo. Furthermore, LMP2A is capable of providing B cells with survival signals in the absence of normal BCR signaling. These data show that LMP2A may help EBV-infected cells to persist in vivo. This review discusses the advances that have been made in our understanding of LMP2A and the effects it has on B cell development, activation, and viral latency.
爱泼斯坦-巴尔病毒（EBV）感染循环通过口腔上皮的B淋巴细胞，并在一部分成熟记忆B细胞中建立终身潜伏感染。在这些潜伏感染的B细胞中，EBV表现出有限的基因表达，潜伏膜蛋白2A（LMP2A）是最常检测到的转录本。这种持续表达，加上许多关于LMP2A在体外和体内功能的研究，表明LMP2A在控制病毒潜伏的某些方面发挥作用。病毒潜伏的建立和维持需要对正常B细胞信号传导和功能进行精确调控。LMP2A能够在体外阻断正常B细胞信号转导，提示LMP2A可能在体内调节从潜伏状态的裂解激活。此外，LMP2A能够在缺乏正常BCR信号的情况下为B细胞提供生存信号。这些数据表明LMP2A可能有助于EBV感染的细胞在体内持续存在。本综述讨论了我们对LMP2A的理解以及它对B细胞发育、激活和病毒潜伏的影响方面取得的进展。
