Okamoto Toru, Suzuki Tatsuya, Kusakabe Shinji, Tokunaga Makoto, Hirano Junki, Miyata Yuka, Matsuura Yoshiharu
Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Viruses. 2017 Aug 28;9(9):243. doi: 10.3390/v9090243.
Apoptosis is a type of programmed cell death that regulates cellular homeostasis by removing damaged or unnecessary cells. Its importance in host defenses is highlighted by the observation that many viruses evade, obstruct, or subvert apoptosis, thereby blunting the host immune response. Infection with Flaviviruses such as Japanese encephalitis virus (JEV), Dengue virus (DENV) and West Nile virus (WNV) has been shown to activate several signaling pathways such as endoplasmic reticulum (ER)-stress and AKT/PI3K pathway, resulting in activation or suppression of apoptosis in virus-infected cells. On the other hands, expression of some viral proteins induces or protects apoptosis. There is a discrepancy between induction and suppression of apoptosis during flavivirus infection because the experimental situation may be different, and strong links between apoptosis and other types of cell death such as necrosis may make it more difficult. In this paper, we review the effects of apoptosis on viral propagation and pathogenesis during infection with flaviviruses.
细胞凋亡是一种程序性细胞死亡,通过清除受损或不必要的细胞来调节细胞内环境稳态。许多病毒逃避、阻碍或破坏细胞凋亡,从而削弱宿主免疫反应,这一现象凸显了细胞凋亡在宿主防御中的重要性。已表明感染黄病毒,如日本脑炎病毒(JEV)、登革病毒(DENV)和西尼罗河病毒(WNV)会激活多种信号通路,如内质网(ER)应激和AKT/PI3K通路,从而导致病毒感染细胞中细胞凋亡的激活或抑制。另一方面,一些病毒蛋白的表达会诱导或保护细胞凋亡。在黄病毒感染期间,细胞凋亡的诱导和抑制之间存在差异,因为实验情况可能不同,而且细胞凋亡与其他类型的细胞死亡(如坏死)之间的紧密联系可能使其更加复杂。在本文中,我们综述了细胞凋亡对黄病毒感染期间病毒传播和发病机制的影响。