Young L S, Rowe M
Department of Cancer Studies, University of Birmingham Medical School, UK.
Semin Cancer Biol. 1992 Oct;3(5):273-84.
Epstein-Barr virus (EBV) is implicated in the pathogenesis of a number of human lymphoid malignancies, including the immunoblastic B lymphomas that arise in immunocompromised individuals, Burkitt's lymphoma, Hodgkin's disease, and certain T cell lymphomas. The immunoblastic lymphomas are most likely a direct consequence of EBV-driven B cell lymphoproliferation that would in normal circumstances be eliminated by virus-specific cell-mediated immune responses. The other EBV-associated malignancies arise in individuals with more or less intact cellular immune responses and appear to have a complex multi-step pathogenesis. Throughout the EBV-positive lymphoid malignancies there is an intimate association between tumour cell phenotype and virus latent gene expression, with each of the three forms of latency seen in in vitro models being exemplified in vivo. Tumours with these different forms of virus latency will differ in their susceptibility to EBV-specific immune T cell control.
爱泼斯坦-巴尔病毒（EBV）与多种人类淋巴系统恶性肿瘤的发病机制有关，包括免疫功能低下个体中出现的免疫母细胞性B淋巴瘤、伯基特淋巴瘤、霍奇金病以及某些T细胞淋巴瘤。免疫母细胞性淋巴瘤很可能是EBV驱动的B细胞淋巴增殖的直接后果，而在正常情况下，这种增殖会被病毒特异性细胞介导的免疫反应消除。其他与EBV相关的恶性肿瘤则发生在细胞免疫反应或多或少保持完整的个体中，其发病机制似乎较为复杂，涉及多个步骤。在所有EBV阳性的淋巴系统恶性肿瘤中，肿瘤细胞表型与病毒潜伏基因表达之间存在密切关联，体外模型中所见的三种潜伏形式在体内均有实例体现。具有这些不同病毒潜伏形式的肿瘤对EBV特异性免疫T细胞控制的敏感性会有所不同。
