Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.
Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.
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DOI：
10.1016/j.virol.2011.12.018
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发表时间：
2012-03-15
期刊：
影响因子：
3.7
通讯作者：
Roman A
中科院分区：
文献类型：
--
作者：
Klingelhutz AJ;Roman A
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揭示中。其原因包括：a)癌蛋白是多功能的，b)细胞相互作用蛋白的列表不断增长，c)不止一种细胞蛋白可能与癌蛋白的给定区域结合，d)有关相应非致癌pv编码的蛋白质的信息有限。本综述的观点是比较致癌的人hpv（称为高危hpv）编码的病毒E6和E7蛋白与非致癌的人hpv（称为低风险hpv）编码的病毒E6和E7蛋白的活性，试图从致癌功能中梳理出病毒生命周期相关的功能。这篇综述将强调从引起粘膜/生殖道癌症的hpv细胞培养研究中获得的经验教训。
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.
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