Regulation of cell survival and death during Flavivirus infections

• 作者: Beata Sadigh Emmanuel Datan Richard A Lockshin Sounak Ghosh Roy Zahra Zakeri
• 来源期刊: 世界生物化学杂志：英文版（电子版）
• 学科: 医学
• 关键词: FLAVIVIRUS Dengue VIRUS West NILE VIRUS Japanese encephalitis VIRUS Programmed cell DEATH Apoptosis EXTRINSIC PATHWAY Intrinsic PATHWAY Autophagy Necrosis
• 年，卷（期）: 2014,（2）
• 页码范围: 93-105
• 页数: 13页
• 分类号: R373

摘要

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 α 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.