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Regulation of Apoptosis during Flavivirus Infection

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

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资金

  1. Program for Basic and Clinical Research on Hepatitis from Japan Agency for Medical Research and development (AMED) [17fk0210206h0002, 17fk0210305h0003, 17fk0210210h0002, 17fk0210209h0502, 17fk0210304h0003]
  2. Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan [16H06432, 16H06429, 16K21723, 15H04736, 16K19139]
  3. Grants-in-Aid for Scientific Research [15H04736, 16H06429, 16H06432, 16K19139] Funding Source: KAKEN

向作者/读者索取更多资源

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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