Hui Kwai Fung, Yiu Stephanie Pei Tung, Tam Kam Pui, Chiang Alan Kwok Shing
Department of Paediatrics and Adolescent Medicine, Li Ka Shing Faculty of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, Hong Kong.
Center for Nasopharyngeal Carcinoma Research, The University of Hong Kong, Hong Kong, Hong Kong.
Front Oncol. 2019 Feb 26;9:81. doi: 10.3389/fonc.2019.00081. eCollection 2019.
Epstein-Barr virus (EBV) is strongly associated with a spectrum of EBV-associated lymphoproliferative diseases (EBV-LPDs) ranging from post-transplant lymphoproliferative disorder, B cell lymphomas (e.g., endemic Burkitt lymphoma, Hodgkin lymphoma, and diffuse large B cell lymphoma) to NK or T cell lymphoma (e.g., nasal NK/T-cell lymphoma). The virus expresses a number of latent viral proteins which are able to manipulate cell cycle and cell death processes to promote survival of the tumor cells. Several FDA-approved drugs or novel compounds have been shown to induce killing of some of the EBV-LPDs by inhibiting the function of latent viral proteins or activating the viral lytic cycle from latency. Here, we aim to provide an overview on the mechanisms by which EBV employs to drive the pathogenesis of various EBV-LPDs and to maintain the survival of the tumor cells followed by a discussion on the development of viral-targeted strategies based on the understanding of the patho-mechanisms.
爱泼斯坦-巴尔病毒(EBV)与一系列爱泼斯坦-巴尔病毒相关淋巴增殖性疾病(EBV-LPDs)密切相关,这些疾病包括移植后淋巴增殖性疾病、B细胞淋巴瘤(如地方性伯基特淋巴瘤、霍奇金淋巴瘤和弥漫性大B细胞淋巴瘤)以及NK或T细胞淋巴瘤(如鼻NK/T细胞淋巴瘤)。该病毒表达多种潜伏性病毒蛋白,这些蛋白能够操纵细胞周期和细胞死亡过程,以促进肿瘤细胞的存活。已证明几种FDA批准的药物或新型化合物可通过抑制潜伏性病毒蛋白的功能或从潜伏期激活病毒裂解周期来诱导杀死某些EBV-LPDs。在此,我们旨在概述EBV驱动各种EBV-LPDs发病机制并维持肿瘤细胞存活的机制,随后基于对发病机制的理解讨论病毒靶向策略的发展。