Kaposi sarcoma-associated herpesvirus (KSHV) is the etiologic agent of several malignancies of endothelial and B-cell origin. The fact that latently infected tumor cells in these malignancies do not express classical viral oncogenes suggests that pathogenesis of KSHV-associated disease results from multistep processes that, in addition to constitutive viral gene expression, may require accumulation of cellular alterations. Heritable changes of the epigenome have emerged as an important co-factor that contributes to the pathogenesis of many non-viral cancers. Since KSHV encodes a number of factors that directly or indirectly manipulate host cell chromatin, it is an intriguing possibility that epigenetic reprogramming also contributes to the pathogenesis of KSHV-associated tumors. The fact that heritable histone modifications have also been shown to regulate viral gene expression programs in KSHV-infected tumor cells underlines the importance of epigenetic control during latency and tumorigenesis. We here review what is presently known about the role of epigenetic regulation of viral and host chromatin in KSHV infection and discuss how viral manipulation of these processes may contribute to the development of KSHV-associated disease.

中文翻译：

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卡波西氏肉瘤相关疱疹病毒感染和相关疾病的表观遗传控制。

卡波氏肉瘤相关疱疹病毒（KSHV）是内皮和B细胞起源的几种恶性肿瘤的病因。在这些恶性肿瘤中潜在感染的肿瘤细胞不表达经典病毒致癌基因这一事实表明，KSHV相关疾病的发病机理是由多步过程导致的，除了组成型病毒基因表达外，还可能需要细胞改变的积累。表观基因组的遗传变化已作为重要的辅助因素出现，这是许多非病毒性癌症的发病机理。由于KSHV编码直接或间接操纵宿主细胞染色质的许多因素，因此表观遗传重编程也可能导致与KSHV相关的肿瘤的发病机理，这是一个令人着迷的可能性。可遗传的组蛋白修饰也已被证明可以调节KSHV感染的肿瘤细胞中病毒基因表达程序，这一事实强调了潜伏期和肿瘤发生过程中表观遗传控制的重要性。我们在这里回顾了目前有关表观遗传调控病毒和宿主染色质在KSHV感染中的作用的知识，并讨论了这些过程的病毒操纵如何可能有助于KSHV相关疾病的发展。