Centre for Human Virology and the School of Cancer Sciences, University of Birmingham, Birmingham, UK.
J Pathol. 2015 Jan;235(2):312-22. doi: 10.1002/path.4459.
Since the discovery in 1964 of the Epstein-Barr virus (EBV) in African Burkitt lymphoma, this virus has been associated with a remarkably diverse range of cancer types. Because EBV persists in the B cells of the asymptomatic host, it can easily be envisaged how it contributes to the development of B-cell lymphomas. However, EBV is also found in other cancers, including T-cell/natural killer cell lymphomas and several epithelial malignancies. Explaining the aetiological role of EBV is challenging, partly because the virus probably contributes differently to each tumour and partly because the available disease models cannot adequately recapitulate the subtle variations in the virus-host balance that exist between the different EBV-associated cancers. A further challenge is to identify the co-factors involved; because most persistently infected individuals will never develop an EBV-associated cancer, the virus cannot be working alone. This article will review what is known about the contribution of EBV to lymphoma development.
自 1964 年在非洲伯基特淋巴瘤中发现 EBV（Epstein-Barr 病毒）以来，这种病毒已与多种癌症类型相关联。由于 EBV 持续存在于无症状宿主的 B 细胞中，因此很容易想象它如何促进 B 细胞淋巴瘤的发展。然而，EBV 也存在于其他癌症中，包括 T 细胞/自然杀伤细胞淋巴瘤和几种上皮恶性肿瘤。解释 EBV 的病因作用具有挑战性，部分原因是病毒可能对每种肿瘤的作用不同，部分原因是现有的疾病模型不能充分再现不同 EBV 相关癌症之间存在的病毒-宿主平衡的细微变化。另一个挑战是确定涉及的共同因素；因为大多数持续感染的个体永远不会发展为 EBV 相关的癌症，所以病毒不能单独起作用。本文将回顾 EBV 对淋巴瘤发展的贡献。
