Human Papillomaviruses (HPVs) are double-stranded DNA viruses, that infect epithelial cells and are etiologically involved in the development of human cancer. Today, over 200 types of human papillomaviruses are known. They are divided into low-risk and high-risk HPVs depending on their potential to induce carcinogenesis, driven by two major viral oncoproteins, E6 and E7. By interacting with cellular partners, these proteins are involved in interdependent viral and cell cycles in stratified differentiating epithelium, and concomitantly induce epigenetic changes in infected cells and those undergoing malignant transformation. E6 and E7 oncoproteins interact with and/or modulate expression of many proteins involved in epigenetic regulation, including DNA methyltransferases, histone-modifying enzymes and subunits of chromatin remodeling complexes, thereby influencing host cell transcription program. Furthermore, HPV oncoproteins modulate expression of cellular micro RNAs. Most of these epigenetic actions in a complex dynamic interplay participate in the maintenance of persistent infection, cell transformation, and development of invasive cancer by a considerable deregulation of tumor suppressor and oncogenes. In this study, we have undertaken to discuss a number of studies concerning epigenetic regulations in HPV-dependent cells and to focus on those that have biological relevance to cancer progression.

中文翻译：

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人乳头瘤病毒在表观遗传学规定中。

人乳头瘤病毒（HPV）是双链DNA病毒，可感染上皮细胞并在病因上参与人类癌症的发展。如今，已知超过200种人类乳头瘤病毒。根据它们诱导致癌作用的潜力，将它们分为低风险和高风险HPV，这是由两种主要的病毒癌蛋白E6和E7驱动的。通过与细胞伴侣相互作用，这些蛋白质参与了分层分化上皮细胞的相互依赖的病毒和细胞周期，并同时在感染细胞和经历恶性转化的细胞中诱导表观遗传学变化。E6和E7癌蛋白与许多参与表观遗传调控的蛋白质相互作用和/或调节其表达，包括DNA甲基转移酶，组蛋白修饰酶和染色质重塑复合物的亚基，从而影响宿主细胞的转录程序。此外，HPV癌蛋白调节细胞微RNA的表达。在复杂的动态相互作用中，大多数这些表观遗传行为通过显着放松肿瘤抑制因子和癌基因参与维持持续感染，细胞转化和浸润性癌症的发展。在这项研究中，我们进行了讨论有关HPV依赖性细胞中表观遗传调控的许多研究，并集中于那些与癌症进展具有生物学相关性的研究。肿瘤抑制因子和致癌基因的显着失控，导致侵袭性癌症的发生和发展。在这项研究中，我们进行了讨论有关HPV依赖性细胞中表观遗传调控的许多研究，并集中于那些与癌症进展具有生物学相关性的研究。肿瘤抑制因子和致癌基因的显着失控，导致侵袭性癌症的发生和发展。在这项研究中，我们进行了讨论有关HPV依赖性细胞中表观遗传调控的许多研究，并集中于那些与癌症进展具有生物学相关性的研究。