School of Life Sciences, University of Sussex, Brighton BN1 9QG, UK.
Curr Opin Virol. 2017 Oct;26:149-155. doi: 10.1016/j.coviro.2017.08.004. Epub 2017 Sep 12.
The oncogenic Epstein-Barr virus (EBV) growth transforms B cells and drives lymphoma and carcinoma development. The virus encodes four key transcription factors (EBNA2, EBNA3A, EBNA3B and EBNA3C) that hijack host cell factors to bind gene control elements and reprogramme infected B cells. These viral factors predominantly target long-range enhancers to alter the expression of host cell genes that control B cell growth and survival and facilitate virus persistence. Enhancer and super-enhancer binding by these EBNAs results in large-scale reorganisation of three-dimensional enhancer-promoter architecture to drive the overexpression of oncogenes, the silencing of tumour suppressors and the modulation of transcription, cell-cycle progression, migration and adhesion.
致癌的 EBV（Epstein-Barr 病毒）生长转化 B 细胞，并驱动淋巴瘤和癌的发展。该病毒编码四个关键的转录因子（EBNA2、EBNA3A、EBNA3B 和 EBNA3C），这些因子劫持宿主细胞因子来结合基因控制元件并重新编程感染的 B 细胞。这些病毒因子主要靶向长距离增强子，以改变控制 B 细胞生长和存活的宿主细胞基因的表达，并促进病毒的持续存在。这些 EBNAs 与增强子和超级增强子的结合导致三维增强子-启动子结构的大规模重组，从而驱动癌基因的过度表达、肿瘤抑制基因的沉默以及转录、细胞周期进程、迁移和黏附的调节。
