期刊
NEUROPATHOLOGY
卷 32, 期 4, 页码 398-405出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1440-1789.2011.01275.x
关键词
apoptosis; immunohistochemistry; mice; ubiquitinated proteins; West Nile virus
资金
- Ministry of Education, Culture, Sports, Science and Technology
- Ministry of Health, Labor and Welfare, Japan
- Japan Health Sciences Foundation
- Program of Founding Research Centers for Emerging and Reemerging Infectious Diseases, MEXT, Japan
- Grants-in-Aid for Scientific Research [23658247] Funding Source: KAKEN
West Nile virus (WNV) belongs to the Flaviviridae family of viruses and has emerged as a significant cause of viral encephalitis in humans, animals and birds. It has been reported that WNV replication directly induces neuronal injury, followed by neuronal cell death proven as apoptosis. Therefore, it is important to understand the mechanism of neuronal apoptosis caused by this virus to develop strategies to control its pathogenicity. Accumulation of ubiquitinated abnormal proteins has been reported to be associated with neuronal apoptosis in some pathological conditions. A lot of cellular stresses prevent cellular protein quality control mechanisms, resulting in the accumulation of ubiquitinated abnormal proteins. To obtain a better understanding of the mechanisms of WNV-induced neuronal apoptosis, we evaluated the accumulation of ubiquitinated proteins in the WNV-infected neuronal cells. We have observed that WNV infection caused massive neuronal injury in the brains of mice. Viral antigen was detected in the neuronal cytoplasm of the cells exhibiting neuronal apoptosis. Notably, ubiquitinated proteins were detected in WNV-infected neuronal cells. In addition, accumulation of ubiquitinated proteins was markedly enhanced in mouse neuroblastoma, Neuro-2a cells after WNV infection. Our histopathological and in vitro studies suggest that accumulation of ubiquitinated proteins in neuronal cells might be associated with neuronal apoptosis caused by WNV infection.
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