Human Oncogenic Herpesvirus and Post-translational Modifications - Phosphorylation and SUMOylation.
Human Oncogenic Herpesvirus and Post-translational Modifications - Phosphorylation and SUMOylation.
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DOI：
10.3389/fmicb.2016.00962
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发表时间：
2016
影响因子：
5.2
通讯作者：
Robertson ES
中科院分区：
文献类型：
--
作者：
Chang PC;Campbell M;Robertson ES
病原体，特别是病毒，进化出利用细胞机制促进其生存和繁殖的能力。翻译后修饰（PTMs），尤其是磷酸化和SUMO化，可逆地调节靶蛋白的功能和相互作用，是细胞信号转导途径中最重要的特征之一。PTM依赖性事件也是病毒最喜欢的靶标之一。在七种明确的人类致癌病毒中，B型肝炎病毒（HBV）、丙型肝炎病毒（HCV）、EB病毒（EBV）、卡波西肉瘤相关疱疹病毒（KSHV）、人乳头瘤病毒（HPV）、人T淋巴细胞病毒-1（HTLV-1）和默克尔细胞多瘤病毒（MCPyV），其中两种是疱疹病毒。疱疹病毒的生命周期由潜伏期和裂解期组成，这些状态之间的快速转换包括病毒基因组从异染色质到常染色质的整体重塑。裂解复制和潜伏期之间的平衡对于疱疹病毒通过病毒繁殖和逃避宿主免疫应答的组合来维持持续感染是必不可少的，这因此可能有助于肿瘤发生。毫不奇怪，PTM的快速可逆性，特别是SUMO化，一种表观遗传学调节染色质结构的修饰，是致癌疱疹病毒宿主的主要劫持靶标。在这篇简短的综述中，我们总结了疱疹病毒通过PTM参与宿主免疫组分的各种方式，重点是磷酸化和SUMO化。
Pathogens, especially viruses, evolve abilities to utilize cellular machineries to facilitate their survival and propagation. Post-translational modifications (PTMs), especially phosphorylation and SUMOylation, that reversibly modulate the function and interactions of target proteins are among the most important features in cell signaling pathways. PTM-dependent events also serve as one of the favorite targets for viruses. Among the seven unambiguous human oncogenic viruses, hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV), human papillomavirus (HPV), Human T lymphotrophic virus-1 (HTLV-1), and Merkel cell polyomavirus (MCPyV), two are herpesviruses. The life cycle of herpesviruses consists of latent and lytic phases and the rapid switch between these states includes global remodeling of the viral genome from heterochromatin-to-euchromatin. The balance between lytic replication and latency is essential for herpesvirus to maintain a persistent infection through a combination of viral propagation and evasion of the host immune response, which consequently may contribute to tumorigenesis. It is no surprise that the swift reversibility of PTMs, especially SUMOylation, a modification that epigenetically regulates chromatin structure, is a major hijack target of the host for oncogenic herpesviruses. In this brief review, we summarize the varied ways in which herpesviruses engage the host immune components through PTMs, focusing on phosphorylation and SUMOylation.