碩士 / 國立成功大學 / 生物科技研究所碩博士班 / 95 / Infectious pancreatic necrosis virus (IPNV) is a fish-derived pathogen and is the prototype of the Birnaviridae virus family. Birnaviruses possess a bi-segmented, double-stranded RNA genome contained within a medium-sized, unenveloped, icosahedral capsid.
In this thesis, we found that IPNV infection can induce the mitochondrial permeability change between 6h and 8 h post-infection (p.i.) time, which also corresponded to activate the initiator caspase-9 and effector caspase-3 for triggering cell death. Then IPNV-induced loss of mitochondrial membrane potential (MMP) can be inhibited by treatment with mitochondrial permeability transition pore inhibitor Bongkrek acid (20ug/ml) (BKA). Furthermore, the viral anti-apoptotic member IPNV VP5 can block IPNV-induced mitochondria- mediated cell death in CHSE-214 cells. Moreover, the IPNV-infection CHSE-214 can up-regulate the ER stress marker GRP 78, at middle apoptotic stage, in CHSE-214 cells.
Taken our results suggest that IPNV induces host cell apoptosis may through mitochondria-mediated death pathway, this finding may provide an important insight into the control of IPNV infection.
| Identifer | oai:union.ndltd.org:TW/095NCKU5111014 |
| Date | January 2007 |
| Creators | Po-Chun Chen, 陳栢均 |
| Contributors | Jiann-Ruey Hong, 洪健睿 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 87 |
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