Zalani S, Holley-Guthrie E, Kenney S
Department of Medicine, University of North Carolina 27599, USA.
Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9194-9. doi: 10.1073/pnas.93.17.9194.
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.
爱泼斯坦-巴尔病毒（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）以及B细胞恶性肿瘤相关的人类疱疹病毒。了解病毒潜伏如何被破坏是疱疹病毒生物学的核心问题。上皮细胞是人类宿主体内EBV裂解复制的主要部位，病毒再激活发生在与EBV相关的鼻咽癌中。已知单个病毒立即早期蛋白BZLF1的表达足以启动B细胞从潜伏感染到裂解感染的转变。因此，BZLF1转录的细胞调控被认为在调节病毒潜伏的严格性中起关键作用。在这里，我们意外地发现，另一种病毒立即早期蛋白BRLF1的表达可以以上皮细胞特异性方式破坏病毒潜伏。因此，导致EBV潜伏破坏的机制似乎具有细胞类型特异性。
