Sun Di, Wen Xingjian, Wang Mingshu, Mao Sai, Cheng Anchun, Yang Xiaoyao, Jia Renyong, Chen Shun, Yang Qiao, Wu Ying, Zhu Dekang, Liu Mafeng, Zhao Xinxin, Zhang Shaqiu, Wang Yin, Xu Zhiwen, Chen Zhengli, Zhu Ling, Luo Qihui, Liu Yunya, Yu Yanling, Zhang Ling, Chen Xiaoyue
Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, China.
Front Microbiol. 2019 Sep 3;10:2032. doi: 10.3389/fmicb.2019.02032. eCollection 2019.
Cell death is a fundamental process in maintaining cellular homeostasis, which can be either accidental or programed. Programed cell death depends on the specific signaling pathways, resulting in either lytic or non-lytic morphology. It exists in two primary forms: apoptosis and autophagic cell death. Apoptosis is a non-lytic and selective cell death program, which is executed by caspases in response to non-self or external stimuli. In contrast, autophagy is crucial for maintaining cellular homeostasis via the degradation and recycling of cellular components. These two mechanisms also function in the defense against pathogen attack. However, picornaviruses have evolved to utilize diverse strategies and target critical components to regulate the apoptotic and autophagic processes for optimal replication and the release from the host cell. Although an increasing number of investigations have shown that the apoptosis and autophagy are altered in picornavirus infection, the mechanism by which viruses take advantage of these two processes remains unknown. In this review, we discuss the mechanisms of picornavirus executes cellular apoptosis and autophagy at the molecular level and the relationship between these interactions and viral pathogenesis.
细胞死亡是维持细胞内稳态的一个基本过程，它可以是意外发生的，也可以是程序性的。程序性细胞死亡依赖于特定的信号通路，会导致溶解性或非溶解性形态。它主要以两种形式存在：凋亡和自噬性细胞死亡。凋亡是一种非溶解性的选择性细胞死亡程序，由半胱天冬酶响应非自身或外部刺激而执行。相比之下，自噬对于通过细胞成分的降解和再循环来维持细胞内稳态至关重要。这两种机制在抵御病原体攻击中也发挥作用。然而，小核糖核酸病毒已经进化出利用多种策略并靶向关键成分来调节凋亡和自噬过程，以实现最佳复制和从宿主细胞中释放。尽管越来越多的研究表明小核糖核酸病毒感染会改变凋亡和自噬，但病毒利用这两个过程的机制仍然未知。在这篇综述中，我们在分子水平上讨论小核糖核酸病毒执行细胞凋亡和自噬的机制，以及这些相互作用与病毒发病机制之间的关系。
