Molecular Mechanism Study of Endoplasmic Reticulum Stress-Induced Cell Death and Relationship with Immune Response by Nervous Necrosis Virus Infection

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Project title

Code/計畫編號

NSC98-2313-B019-006

Translated Name/計畫中文名

神經壞死病毒誘發內質網壓力造成細胞凋亡與免疫之間的機制研究

Project Coordinator/計畫主持人

Ming-Wei Lu

Funding Organization/主管機關

National Science and Technology Council

Department/Unit

Department of Aquaculture

Website

https://www.grb.gov.tw/search/planDetail?id=1870639

Year

2009

Start date/計畫起

01-06-2009

Expected Completion/計畫迄

31-07-2010

Bugetid/研究經費

1300千元

ResearchField/研究領域

漁業
生物技術(農)

"病毒性神經壞死症(viral nervous necrosis; VNN)為經由魚類野田病毒(Betanodaviruses)感染所引起的一種神經性疾病，罹病的魚類將出現泳動異常及體色變深等病徵，並於腦部及視網膜出現壞死，硬骨魚若在仔魚及稚魚時期感染神經壞死病毒會引起大量死亡，造成水產養殖業相當大的經濟衝擊，但是目前對於魚類野田病毒的研究仍未詳盡，因此瞭解病毒的分子調控機制將有助於解析病毒的感染與致病過程。在先前的研究報告中，我們已經成功開發利用斑馬魚來建立神經壞死病毒的感染模式，這也是首次神經壞死病毒所建立的感染模式，藉由這樣的模式，我們初步發現，神經壞死病毒的急性與持續性感染與先天免疫有很大的關係，除此之外，在活體及細胞株內感染中也發現細胞凋亡的現象，藉由初步的實驗證明，這樣的細胞凋亡與內質網壓力有很大的關連性。在本計畫中，我們將著重於探討幾項重要的因子如病毒所誘發ER stress於病毒之複製及病毒引發免疫系統之間的關連性，病毒所誘發之autophagy formantion，對於神經壞死病毒決定走向急性感染(acute infection)或是潛伏性感染(persistent infection)之影響程度如何。此項研究將於石斑魚細胞株與模式魚種斑馬魚內完成。其實驗結果將提供RNA病毒對於控制宿主細胞走向急性感染或轉向潛伏性感染所引起魚類神經性疾病有更深入的瞭解。更希望此結果能有助於一般病毒感染機制上之研究。" "Betanodaviruses cause viral nervous necrosis (VNN), an infectious neuropathological condition of fish that is characterized by necrosis of the central nervous system including the brain and retina, and which is accompanied by clinical signs such as abnormal swimming behavior and development of a darker body color. The disease is of global economic importance, being capable of causing mass mortality in larval and juvenile populations of several teleost species. Despite this severe impact on the aquaculture industry, betanodaviruses have not been well studied. Characterization of the viral molecular regulation processes would aid in deciphering the mechanism(s) of viral pathogenesis and infection. In our previously study, we had established an infection model of NNV by using zebrafish. This is also the first case to establish a NNV infection model. We also used this infection model to study to immune response and apoptosis regulation. According the preliminary data, we found that the NNV susceptible is related to innate immunity. Moreover, we also observed the apoptosis event in infected zebrafish brain and GF-1 cell. The apoptosis event is related to ER-stress according the western and RT-PCR results. In this project, we want to know this necrotic virus how to determine going to acute or persistent infection that the some crucial factors such as virus-induced ER stress and immune responses, virus-induced autophagy, will be characterized in vitro and in vivo. Our observations will provide the further insight into RNA viruses-induced switching of the acute or persistent infection in pathogenesis and disease control. These studies could also give a general mechanism in virus infection and pathogenesis."

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Molecular Mechanism Study of Endoplasmic Reticulum Stress-Induced Cell Death and Relationship with Immune Response by Nervous Necrosis Virus Infection

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