PDF(Pubmed)
Abstract：
During viral infection, the innate immune system utilizes a variety of specific intracellular sensors to detect virus-derived nucleic acids and activate a series of cellular signaling cascades that produce type I IFNs and proinflammatory cytokines and chemokines. Kaposi\'s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus that has been associated with a variety of human malignancies, including Kaposi\'s sarcoma, primary effusion lymphoma, and multicentric Castleman disease. Infection with KSHV activates various DNA sensors, including cGAS, STING, IFI16, and DExD/H-box helicases. Activation of these DNA sensors induces the innate immune response to antagonize the virus. To counteract this, KSHV has developed countless strategies to evade or inhibit DNA sensing and facilitate its own infection. This review summarizes the major DNA-triggered sensing signaling pathways and details the current knowledge of DNA-sensing mechanisms involved in KSHV infection, as well as how KSHV evades antiviral signaling pathways to successfully establish latent infection and undergo lytic reactivation.
摘要：
在病毒感染期间,先天性免疫系统利用各种特定的细胞内传感器来检测病毒衍生的核酸并激活一系列产生I型IFN和促炎细胞因子和趋化因子的细胞信号级联。卡波西肉瘤相关疱疹病毒（KSHV）是一种致癌双链DNA病毒，与多种人类恶性肿瘤有关。包括卡波西肉瘤,原发性渗出性淋巴瘤，和多中心Castleman病.KSHV感染激活了各种DNA传感器，包括CGAS，STING,IFI16和DExD/H-box解旋酶。这些DNA传感器的激活诱导先天性免疫应答以拮抗病毒。为了抵消这一点，KSHV已经开发了无数的策略来逃避或抑制DNA感应并促进其自身的感染。这篇综述总结了主要的DNA触发感应信号通路，并详细介绍了KSHV感染中涉及的DNA感应机制的最新知识。以及KSHV如何逃避抗病毒信号通路以成功建立潜伏感染并进行裂解剂再激活。
