期刊
VIRUSES-BASEL
卷 9, 期 9, 页码 -出版社
MDPI AG
DOI: 10.3390/v9090243
关键词
apoptosis; B-cell lymphoma 2 (BCL2); flavivirus; dengue virus; Japanese encephalitis virus; West Nile virus
类别
资金
- Program for Basic and Clinical Research on Hepatitis from Japan Agency for Medical Research and development (AMED) [17fk0210206h0002, 17fk0210305h0003, 17fk0210210h0002, 17fk0210209h0502, 17fk0210304h0003]
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan [16H06432, 16H06429, 16K21723, 15H04736, 16K19139]
- Grants-in-Aid for Scientific Research [15H04736, 16H06429, 16H06432, 16K19139] Funding Source: KAKEN
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.
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