碩士 / 國立臺灣大學 / 動物學研究所 / 97 / Nervous necrosis virus (NNV) is a positive single-stranded RNA virus. NNV infection was reported to induce the loss of mitochondria membrane potential. Autophagy is a unique membrane traffic system for engulfing long-lived proteins and organelles to maintain homeostasis of cellular energy during starvation. This research first reported the interaction between NNV and autophagy in fish cells. After transfection of pEGFP-LC3 plasmids, fluorescence of autophagosomes was observed in NNV-infected cells. Quantitative analysis of ATP by chemoiluminescence, ATP was found to decrease gradually after NNV infection. When viral protein translation was inhibited by cycloheximide (CHX) treatment, the level of ATP restored to the original level of non-infected cells, indicating that NNV replication could decrease ATP of infected cell. By the way, the level of autophagy could be induced by NNV infection, but it was down-regulated when viral protein translation was inhibited by CHX treatment. When the cells were pre-starved to reduce the level of ATP and then infected with NNV, the level of autophagy was higher but the level of viral protein was lower than that in the NNV-infected cells without pre-starvation. Therefore, it is suggested that the up-regulation of autophagosomes in NNV-infected cells was much related with the loss of ATP and less related with ER stress. When NNV-infected cells were separately treated with three autophagy inhibitors, the levels of ATP and the levels of progeny viral titers were lower than that of untreated NNV-infected cells. All the above data suggested that NNV-induced autophagy was helpful to product the cellular ATP and provide the resources for viral replication.
| Identifer | oai:union.ndltd.org:TW/097NTU05312015 |
| Date | January 2009 |
| Creators | Ren-Xiang Wang, 王任翔 |
| Contributors | Shau-Chi Chi, 齊肖琪 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 74 |
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