Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA.
Virology. 2012 Mar 15;424(2):77-98. doi: 10.1016/j.virol.2011.12.018. Epub 2012 Jan 27.
The oncogenic potential of papillomaviruses (PVs) has been appreciated since the 1930s yet the mechanisms of virally-mediated cellular transformation are still being revealed. Reasons for this include: a) the oncoproteins are multifunctional, b) there is an ever-growing list of cellular interacting proteins, c) more than one cellular protein may bind to a given region of the oncoprotein, and d) there is only limited information on the proteins encoded by the corresponding non-oncogenic PVs. The perspective of this review will be to contrast the activities of the viral E6 and E7 proteins encoded by the oncogenic human PVs (termed high-risk HPVs) to those encoded by their non-oncogenic counterparts (termed low-risk HPVs) in an attempt to sort out viral life cycle-related functions from oncogenic functions. The review will emphasize lessons learned from the cell culture studies of the HPVs causing mucosal/genital tract cancers.
自 20 世纪 30 年代以来，人们已经认识到乳头瘤病毒（PV）的致癌潜力，但病毒介导的细胞转化机制仍在不断揭示。造成这种情况的原因包括：a）致癌蛋白具有多功能性，b）有越来越多的细胞相互作用蛋白，c）不止一种细胞蛋白可能与致癌蛋白的特定区域结合，d）对于相应非致癌 PV 编码的蛋白质，信息有限。本综述的观点将对比由致癌性人类乳头瘤病毒（称为高危 HPV）编码的病毒 E6 和 E7 蛋白与由非致癌性 HPV 编码的蛋白的活性（称为低危 HPV），试图将病毒生命周期相关功能与致癌功能区分开来。该综述将重点介绍从引起黏膜/生殖道癌症的 HPV 的细胞培养研究中获得的经验教训。
