Milavetz Barry I, Balakrishnan Lata
Department of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Stop 9037, 501 N. Columbia Rd., Grand Forks, ND, 58202, USA,
Methods Mol Biol. 2015;1238:569-96. doi: 10.1007/978-1-4939-1804-1_30.
DNA tumor viruses including members of the polyomavirus, adenovirus, papillomavirus, and herpes virus families are presently the subject of intense interest with respect to the role that epigenetics plays in control of the virus life cycle and the transformation of a normal cell to a cancer cell. To date, these studies have primarily focused on the role of histone modification, nucleosome location, and DNA methylation in regulating the biological consequences of infection. Using a wide variety of strategies and techniques ranging from simple ChIP to ChIP-chip and ChIP-seq to identify histone modifications, nuclease digestion to genome wide next generation sequencing to identify nucleosome location, and bisulfite treatment to MeDIP to identify DNA methylation sites, the epigenetic regulation of these viruses is slowly becoming better understood. While the viruses may differ in significant ways from each other and cellular chromatin, the role of epigenetics appears to be relatively similar. Within the viral genome nucleosomes are organized for the expression of appropriate genes with relevant histone modifications particularly histone acetylation. DNA methylation occurs as part of the typical gene silencing during latent infection by herpesviruses. In the simple tumor viruses like the polyomaviruses, adenoviruses, and papillomaviruses, transformation of the cell occurs via integration of the virus genome such that the virus's normal regulation is disrupted. This results in the unregulated expression of critical viral genes capable of redirecting cellular gene expression. The redirected cellular expression is a consequence of either indirect epigenetic regulation where cellular signaling or transcriptional dysregulation occurs or direct epigenetic regulation where epigenetic cofactors such as histone deacetylases are targeted. In the more complex herpersviruses transformation is a consequence of the expression of the viral latency proteins and RNAs which again can have either a direct or indirect effect on epigenetic regulation of cellular expression. Nevertheless, many questions still remain with respect to the specific mechanisms underlying epigenetic regulation of the viruses and transformation.
包括多瘤病毒、腺病毒、乳头瘤病毒和疱疹病毒家族成员在内的DNA肿瘤病毒,目前是人们密切关注的对象,因为表观遗传学在控制病毒生命周期以及将正常细胞转化为癌细胞的过程中所起的作用。迄今为止,这些研究主要集中在组蛋白修饰、核小体定位和DNA甲基化在调节感染生物学后果方面的作用。使用从简单的染色质免疫沉淀(ChIP)到ChIP芯片和ChIP测序等多种策略和技术来鉴定组蛋白修饰,通过核酸酶消化到全基因组下一代测序来鉴定核小体定位,以及通过亚硫酸氢盐处理到甲基化DNA免疫沉淀(MeDIP)来鉴定DNA甲基化位点,这些病毒的表观遗传调控正逐渐被人们更好地理解。虽然这些病毒彼此之间以及与细胞染色质可能存在显著差异,但表观遗传学的作用似乎相对相似。在病毒基因组中,核小体通过相关的组蛋白修饰,特别是组蛋白乙酰化,来组织以便适当基因的表达。DNA甲基化是疱疹病毒潜伏感染期间典型基因沉默的一部分。在像多瘤病毒、腺病毒和乳头瘤病毒这样的简单肿瘤病毒中,细胞转化是通过病毒基因组的整合发生的,从而破坏了病毒的正常调控。这导致能够重定向细胞基因表达的关键病毒基因的失控表达。重定向的细胞表达是细胞信号传导或转录失调发生的间接表观遗传调控的结果,或者是诸如组蛋白去乙酰化酶等表观遗传辅因子成为靶点的直接表观遗传调控的结果。在更复杂的疱疹病毒中,转化是病毒潜伏蛋白和RNA表达的结果,这些蛋白和RNA同样可以对细胞表达的表观遗传调控产生直接或间接影响。然而,关于病毒表观遗传调控和转化的具体机制,仍然存在许多问题。