Post-translational modification of target proteins by the Small Ubiquitin-like Modifier (SUMO) plays a critical role in regulation of many cellular processes including transcription, RNA processing, protein trafficking, DNA repair, and chromosome segregation, and is also often hijacked by viral infections. Epstein-Barr Virus (EBV) and Kaposi's sarcoma-associated Herpesvirus (KSHV), two human oncogenic herpesviruses with a typical life cycle of latent and lytic replication, have been shown to be associated with many human cancers. In the past decade, intensive studies have investigated the interplay between tumor virus infection and SUMO-modification. In this review, we summarize the current knowledge as to how SUMOylation can regulate latent and lytic replication of EBV and KSHV, and the strategies by which these oncogenic herpesviruses usurp the SUMO pathways to establish a favorable microenvironment to promote host cell survival and proliferation in latency, and reactivate virion production during lytic replication, which are critical contributors to the development of EBV/KSHV-associated human malignancies.

中文翻译：

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SUMOylation 在人类致癌性疱疹病毒感染中的作用。

小泛素样修饰剂 (SUMO) 对靶蛋白的翻译后修饰在许多细胞过程的调节中起着关键作用，包括转录、RNA 加工、蛋白质运输、DNA 修复和染色体分离，并且还经常被病毒劫持感染。爱泼斯坦-巴尔病毒 (EBV) 和卡波西肉瘤相关疱疹病毒 (KSHV) 这两种人类致癌疱疹病毒具有典型的潜伏和裂解复制生命周期，已被证明与许多人类癌症有关。在过去十年中，大量研究调查了肿瘤病毒感染和 SUMO 修饰之间的相互作用。在这篇综述中，我们总结了关于 SUMOylation 如何调节 EBV 和 KSHV 的潜在和裂解复制的当前知识，