White Martyn K, Khalili Kamel
Center for Neurovirology, Department of Neuroscience, Temple University School of Medicine, 1900 North 12th Street, MS 015-96, Room 203, Philadelphia, PA 19122, USA.
Eur J Cancer. 2005 Nov;41(16):2537-48. doi: 10.1016/j.ejca.2005.08.019. Epub 2005 Oct 10.
JC virus (JCV) is a human polyomavirus that is the etiologic agent of the fatal demyelinating disease of the central nervous system known as progressive multifocal leukoencephalopathy (PML). JCV is also linked to some tumours of the brain and other organs as evidenced by the presence of JCV DNA sequences and the expression of viral proteins in clinical samples. Since JCV is highly oncogenic in experimental animals and transforms cells in culture, it is possible that JCV contributes to the malignant phenotype of human tumours with which it is associated. JCV encodes three non-capsid regulatory proteins: large T-antigen, small t-antigen and agnoprotein that interact with a number of cellular target proteins and interfere with certain normal cellular functions. In this review, we discuss how JCV proteins deregulate signalling pathways especially ones pertaining to transcriptional regulation and cell cycle control. These effects may be involved in the progression of JCV-associated tumours and may represent potential therapeutic targets.
JC病毒（JCV）是一种人类多瘤病毒，是中枢神经系统致命性脱髓鞘疾病——进行性多灶性白质脑病（PML）的病原体。JCV还与一些脑肿瘤和其他器官肿瘤有关，临床样本中JCV DNA序列的存在以及病毒蛋白的表达证明了这一点。由于JCV在实验动物中具有高度致癌性，并能在培养中转化细胞，因此JCV有可能促成与其相关的人类肿瘤的恶性表型。JCV编码三种非衣壳调节蛋白：大T抗原、小t抗原和agnoprotein，它们与许多细胞靶蛋白相互作用，并干扰某些正常细胞功能。在这篇综述中，我们讨论了JCV蛋白如何解除信号通路的调节，尤其是与转录调控和细胞周期控制有关的信号通路。这些效应可能参与了JCV相关肿瘤的进展，并可能代表潜在的治疗靶点。
