白點症病毒（WSSV）是導致白點症（WSD）的病原體，它可以導致高死亡率，並且為世界蝦類養殖界帶來巨大的經濟損失，且白點症病毒如何利用細胞因子幫助其複製至今仍是未知數。SIRT1是NAD +依賴性蛋白質脫乙醯酶，目前已知其在哺乳類動物中，SIRT1為活化或抑制病毒轉錄和複製的調節因子。在本研究中，首先運用實驗室中已建立的白蝦轉錄體資料庫找出LvSIRT1基因。其後研究發現LvSIRT1的脫乙醯酶活性在WSSV複製的早期（2 hpi）和基因組複製階段（12 hpi）被顯著活化。為進一步證實LvSIRT1在白點症病毒複製期間所扮演的角色，本研究用SIRT1活化劑白藜蘆醇（Resveratrol）進行動物實驗，證實LvSIRT1的活化促進了病毒基因表現（ie1、VP28和ICP11）；另外，在使用dsRNA對LvSIRT1進行基因默化，造成病毒複製數顯著下降。本研究運用Sf9昆蟲細胞進行轉染及雙重螢光素酶報告基因檢測實驗，發現過度表現LvSIRT1促進WSSV ie1啟動子的活性，目前已知ie1啟動子p（-268 / + 52）上存在四種轉錄因子結合域，並且透過ie1啟動子之轉錄因子點突變實驗，發現當NF-κB轉錄位點突變後ie1啟動子有更高的活性。總結本研究所得，LvSIRT1應該會促進非NF-κB所調控的WSSV ie1表現。

White spot syndrome virus (WSSV) causes White spot disease (WSD) and has resulted in huge losses in global shrimp aquaculture. Since the mechanisms of cellular factors that modulate replication of white spot syndrome virus (WSSV) still remains unknown. A growing evidence from literature suggests that SIRT1 is NAD+-dependent protein deacetylase that promotes or suppresses the activity of coactivators and cellular transcription factors to regulate several cellular processes. Perhaps WSSV uses SIRT1 to facilitate its replication. Here, we focus on the involvement of SIRT1 in viral replication. In this study, based on our in-house transcriptomic database, LvSIRT1 was identified and characterized from white shrimp. Firstly, we found that the deacetylase activity of LvSIRT1 was significantly induced at the early stage (2 hpi) and the genome replication stage (12 hpi) of WSSV replication, while decreased at the late stage of WSSV replication (24 hpi). To further confirm the roles of LvSIRT1 during WSSV infection, in vivo experiments were conducted with the SIRT1 activator Resveratrol, showed that the activation of LvSIRT1 increased the expression of several WSSV genes (ie1, VP28 and ICP11). Furthermore, after silencing the LvSIRT1 in shrimp using specific dsRNA, the expression of WSSV genome copies was suppressed. Therefore, we suggest that LvSIRT1 might induce WSSV gene transcription to promote WSSV replication. Here we showed that the overexpression of LvSIRT1 let to the controlled enhancement of immediate-early gene ie1 promoter activity by using the dual luciferase assay in Sf9 insect cells. Previous studies have shown the presence of four kinds of transcriptional factor binding motifs in ie1 promoter p(-268/+52). These transcription factors might be regulated by LvSIRT1. In mutation of transcription factor binding sites experiment, luciferase activity was a slight increase at the mNF-κB construct. Furthermore, LvSIRT1 could be involved in the NF-κB-independent transactivation to trigger the expression of WSSV ie1.

何舒莛，白點症病毒於基因體複製時期活化麩醯胺酸代謝作用之氧化與還原路徑，國立成功大學生物科技與產業科學系碩士論文，2018。

曾怡婷，探討蝦類Ras及其下游路徑在感染白點症病毒後代謝路徑轉移過程中所扮演之角色，國立成功大學生物科技與產業科學系碩士論文，2018。

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角色，國立成功大學生物科技研究所碩士論文，2013。

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