Regulation of cell survival and death during Flavivirus infections.
Regulation of cell survival and death during Flavivirus infections.
复制标题
DOI：
10.4331/wjbc.v5.i2.93
复制
发表时间：
2014-05-26
期刊：
影响因子：
--
通讯作者：
Zakeri, Zahra
中科院分区：
文献类型：
--
作者：
Ghosh Roy, Sounak;Sadigh, Beata;Zakeri, Zahra
黄病毒，ss（+）RNA病毒，包括许多人类最重要的病原体。它们的致病性来源于它们感染包括神经元在内的许多类型的细胞、复制并最终杀死细胞的能力。黄病毒可以激活肿瘤坏死因子α和内源性（β-介导的）和外源性凋亡途径。因此，他们可以使用许多方法来激活这些途径。如果病毒载量极高，感染可导致坏死，或者如果细胞凋亡途径被阻断，感染可导致其他类型的细胞死亡。登革热和日本脑炎病毒也可以激活自噬。在这种情况下，自噬暂时地使受感染的细胞免于感染，允许病毒更长时间的繁殖，并且自噬进一步保护细胞免受其他应激，例如由活性氧引起的应激。几种病毒蛋白已被证明可以诱导细胞凋亡或自噬本身，不依赖于其他病毒蛋白的存在。鉴于这些病毒适应和操纵代谢的多功能性，从而控制感染细胞的存活，我们需要更好地了解特定病毒蛋白如何影响凋亡和自噬途径。只有这样，我们才能将它们造成的病理学减少到最低限度。
Flaviviruses, ss(+) RNA viruses, include many of mankind's most important pathogens. Their pathogenicity derives from their ability to infect many types of cells including neurons, to replicate, and eventually to kill the cells. Flaviviruses can activate tumor necrosis factor alpha and both intrinsic (Bax-mediated) and extrinsic pathways to apoptosis. Thus they can use many approaches for activating these pathways. Infection can lead to necrosis if viral load is extremely high or to other types of cell death if routes to apoptosis are blocked. Dengue and Japanese Encephalitis Virus can also activate autophagy. In this case the autophagy temporarily spares the infected cell, allowing a longer period of reproduction for the virus, and the autophagy further protects the cell against other stresses such as those caused by reactive oxygen species. Several of the viral proteins have been shown to induce apoptosis or autophagy on their own, independent of the presence of other viral proteins. Given the versatility of these viruses to adapt to and manipulate the metabolism, and thus to control the survival of, the infected cells, we need to understand much better how the specific viral proteins affect the pathways to apoptosis and autophagy. Only in this manner will we be able to minimize the pathology that they cause.