Shannon-Lowe Claire, Rickinson Alan B, Bell Andrew I
Institute of Immunology and Immunotherapy, The Medical School, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Institute for Cancer and Genomic Sciences, The Medical School, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
Philos Trans R Soc Lond B Biol Sci. 2017 Oct 19;372(1732). doi: 10.1098/rstb.2016.0271.
Epstein-Barr virus (EBV), originally discovered through its association with Burkitt lymphoma, is now aetiologically linked to a remarkably wide range of lymphoproliferative lesions and malignant lymphomas of B-, T- and NK-cell origin. Some occur as rare accidents of virus persistence in the B lymphoid system, while others arise as a result of viral entry into unnatural target cells. The early finding that EBV is a potent B-cell growth transforming agent hinted at a simple oncogenic mechanism by which this virus could promote lymphomagenesis. In reality, the pathogenesis of EBV-associated lymphomas involves a complex interplay between different patterns of viral gene expression and cellular genetic changes. Here we review recent developments in our understanding of EBV-associated lymphomagenesis in both the immunocompetent and immunocompromised host.This article is part of the themed issue 'Human oncogenic viruses'.
爱泼斯坦-巴尔病毒(EBV)最初是通过与伯基特淋巴瘤的关联而被发现的,现在在病因上与多种起源于B细胞、T细胞和NK细胞的淋巴增殖性病变及恶性淋巴瘤有关。一些病变是病毒在B淋巴细胞系统中持续存在的罕见意外结果,而另一些则是病毒进入非天然靶细胞的结果。早期发现EBV是一种强大的B细胞生长转化因子,这暗示了一种简单的致癌机制,即这种病毒可促进淋巴瘤的发生。实际上,EBV相关淋巴瘤的发病机制涉及病毒基因表达的不同模式与细胞遗传变化之间的复杂相互作用。在此,我们综述了在免疫功能正常和免疫功能低下宿主中对EBV相关淋巴瘤发生发展的最新认识。本文是主题为“人类致癌病毒”的特刊的一部分。