Epstein-Barr viral latency is disrupted by the immediate-early BRLF1 protein through a cell-specific mechanism.
Epstein-Barr viral latency is disrupted by the immediate-early BRLF1 protein through a cell-specific mechanism.
复制标题
DOI：
10.1073/pnas.93.17.9194
复制
发表时间：
1996-08
影响因子：
11.1
通讯作者：
S. Zalani;E. Holley-Guthrie;S. Kenney
中科院分区：
文献类型：
--
作者：
S. Zalani;E. Holley-Guthrie;S. Kenney
EB病毒(Epstein-Barr Virus，EBV)是传染性单核细胞增多症的病原体，是一种与上皮细胞恶性肿瘤(鼻咽癌)和B细胞恶性肿瘤相关的人类疱疹病毒。了解病毒潜伏期是如何被破坏的是疱疹病毒生物学的一个中心问题。上皮细胞是人类宿主内EBV裂解复制的主要部位，EBV相关的鼻咽癌中会发生病毒的重新激活。已知，单个病毒即刻早期蛋白BZLF1的表达足以启动B细胞从潜伏感染到裂解感染的转换。因此，细胞对BZLF1转录的调控被认为在调节病毒潜伏期的严格性方面发挥了关键作用。在这里，我们展示了，出乎意料的是，另一种病毒即刻早期蛋白BRLF1的表达可以以上皮细胞特有的方式扰乱病毒潜伏期。因此，导致EBV潜伏期中断的机制似乎与细胞类型有关。
Epstein-Barr virus (EBV), the causative agent of infectious mononucleosis, is a human herpesvirus associated with epithelial cell malignancies (nasopharyngeal carcinoma) as well as B-cell malignancies. Understanding how viral latency is disrupted is a central issue in herpesvirus biology. Epithelial cells are the major site of lytic EBV replication within the human host, and viral reactivation occurs in EBV-associated nasopharyngeal carcinomas. It is known that expression of a single viral immediate-early protein, BZLF1, is sufficient to initiate the switch from latent to lytic infection in B cells. Cellular regulation of BZLF1 transcription is therefore thought to play a key role in regulating the stringency of viral latency. Here we show that, unexpectedly, expression of another viral immediate-early protein, BRLF1, can disrupt viral latency in an epithelial cell-specific fashion. Therefore, the mechanisms leading to disruption of EBV latency appear to be cell-type specific.