| 研究生: |
鄭丞舜 Cheng, Cheng-Shun |
|---|---|
| 論文名稱: |
探討脂質代謝對於白點症病毒複製的重要性 Role of lipid metabolism in white spot syndrome virus replication |
| 指導教授: |
王涵青
Wang, Han-Ching |
| 學位類別: |
碩士 Master |
| 系所名稱: |
生物科學與科技學院 - 生物科技研究所 Institute of Biotechnology |
| 論文出版年: | 2016 |
| 畢業學年度: | 104 |
| 語文別: | 中文 |
| 論文頁數: | 69 |
| 中文關鍵詞: | 白點症病毒 、瓦氏效應 、脂質代謝 |
| 外文關鍵詞: | Penaeus vannamei, White spot syndrome virus, lipolysis, lipogenesis |
| 相關次數: | 點閱:96 下載:2 |
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全球蝦類養殖產業近年因白點症病毒 (White spot syndrome virus, WSSV) 造成極為嚴重之產業損失,因此研究此病毒之致病機轉以尋求防疫策略。本實驗室先前發現,在WSSV感染後12小時 (病毒複製時期) ,病毒會誘導宿主產生類似由癌症於脊椎動物中引發之瓦氏效應,並在24小時後 (感染晚期) 開始釋放病毒。而本實驗室之實驗首次發現在白點症病毒複製時期、感染晚期會進行脂質分解以及脂質生合成現象。本實驗以螢光染色方式,觀測WSSV感染過程中所影響的脂質代謝平衡改變,顯示當WSSV感染後會影響到宿主脂滴分布。而於專一性抑制 Etomoxir 以及 C75 分別抑制 β-oxidation 和 Fatty acid synthesis 之活性後,由結果推測WSSV在病毒複製時期,會促使肝胰腺活化脂質分解,脂肪酸釋放至血淋巴中再由主要感染之組織 (血球及胃) 吸收後,進而用於能量產生,當進入WSSV感染之晚期,雖然病毒促使感染組織中脂質分解,然而組織中脂質之總面積上升,以提供病毒合成所需之材料,完成病毒之組裝及釋放。從本研究成果推測,脂質分解與脂質生合成應主要提供晚期病毒顆粒之膜狀結構合成使用,以完成病毒顆粒的組裝 (morphogenesis) 。未來將進一步探討WSSV所需之關鍵脂質,作為新的治療/預防/篩選標的。
Global metabolic changes in WSSV-infected shrimp were recently clarified by us (using proteomics and metabolomics). In infected shrimp, re-routing host metabolism (analogous to the Warburg effect in cancer cells) increased availability of energy and building blocks in host cells at the genome replication stage (12 hours post infection; hpi). Moreover, WSSV switched lipid metabolism of host from lipolysis at 12 hpi to lipogenesis at 24 hpi and used it to complete the viral replication cycle and morphogenesis. At the replication stage (12 hpi), lipolysis induced by WSSV in hepatopancreas released free fatty acids that were rapidly assimilated by WSSV target tissues (e.g. hemocytes and stomach). Lipolysis switched to hemocytes and stomach until lipid in hepatopamcreas was exhausted at a late stage (24 hpi). Furthermore, beta-oxidation may be triggered during WSSV infection in shrimp. We determined that WSSV may trigger lipolysis in various tissues during viral replication, and that released free fatty acids may be absorbed by target tissues. Conversely, WSSV failed to complete its replication cycle after beta-oxidation was inhibited; this phenomenon was also observed following inhibition of fatty acid synthetase (FAS; a key enzyme of lipogenesis), during WSSV infection. Therefore, we inferred that alteration of lipid metabolism might be essential for WSSV virion formation. Our study provided new insights into important changes in host lipid metabolism triggered by an invertebrate virus.
李春媛,探討榖醯胺酸分解作用於白點症病毒致病機轉知角色,國立成功大學生物科技研究所碩士論文,2015。
謝雲傑,白點症病毒感染對於蝦脂肪酸組成之影響,國立成功大學生物科技研究所碩士論文,2014。
蘇美安,雷帕黴素標靶蛋白訊息傳遞路徑在白點症病毒之致病機轉中所扮演之腳色,國立成功大學生物科技研究所碩士論文,2013。
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