Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Martinistrasse 52, 20252 Hamburg, Germany.
Curr Opin Virol. 2017 Oct;26:104-111. doi: 10.1016/j.coviro.2017.07.018. Epub 2017 Aug 9.
Molecular and epidemiological evidence links Kaposi sarcoma-associated herpesvirus (KSHV) to a number of malignancies of endothelial or B cell origin. As for most virus-associated cancers, however, the tumor initiating and promoting events remain poorly understood. Given the emerging role of epigenetic alterations as drivers of human cancers, an interesting (and as of yet under-explored) hypothesis is that viral manipulation of host cell chromatin may contribute to the pathogenesis of KSHV-associated tumors. We here review the current knowledge regarding the interplay between KSHV-encoded factors and host chromatin and discuss how epigenetic alterations may contribute to the pathogenesis of KSHV-associated tumors.
分子和流行病学证据将卡波西肉瘤相关疱疹病毒(KSHV)与许多内皮或 B 细胞来源的恶性肿瘤联系起来。然而,与大多数病毒相关的癌症一样,肿瘤起始和促进事件仍知之甚少。鉴于表观遗传改变作为人类癌症驱动因素的作用不断凸显,一个有趣的(且尚未充分探索的)假设是,病毒对宿主细胞染色质的操纵可能有助于 KSHV 相关肿瘤的发病机制。在这里,我们回顾了关于 KSHV 编码因子与宿主染色质相互作用的最新知识,并讨论了表观遗传改变如何有助于 KSHV 相关肿瘤的发病机制。