傳染性脾臟及腎臟壞死病毒（Infectious spleen and kidney necrosis virus；ISKNV）屬於虹彩病毒科（Iridoviridae）的巨大細胞屬 （Megalocytivirus）病毒，會造成魚隻器官腫大以及死亡，因此想要了解病毒的機轉與找到防治方法，來解決此問題。本實驗室先前研究證實傳染性脾臟及腎臟壞死病毒感染石斑魚鰭細胞株（GF-1）會誘導ROS上升，添加抗氧化劑後可以降低ROS，並可增加細胞存活率。而ROS會介導自噬作用的產生，因此本研究想探討ISKNV感染GF-1細胞後是否會造成自噬作用的產生，並進一步探討細胞的自噬作用與病毒的表現、複製之間的關聯性如何。在實驗結果中發現，病毒感染可以造成細胞自噬作用，並分別利用UV光、自噬抑制劑3-MA、抗氧化劑NAC和AMPK抑制劑（Compound C）來抑制病毒基因與蛋白質產物之表現與合成。結果發現，病毒複製下降時其所誘導產生的活性氧分子也跟著減少，進而使得自噬作用上游分子發現AMPK活性上升及mTOR活性下降，同時發現減緩了自噬作用進行。目前得知病毒感染時能活化ROS來誘導細胞自噬之啟動。藥劑處理尤其以抗氧化劑NAC處理效果最為顯著。

Infectious spleen and kidney necrosis virus (ISKNV) belongs to the genus Iridoviridae (Megalocytivirus) virus, will cause the fish organ enlargement and death, so that want to know the virus mechanisms to find a way to prevent this problem. Previous studies have confirmed that ISKNV infection grouper fin cell line (GF-1) will induce ROS increase, add antioxidants can reduce ROS, and can increase cell viability. And ROS will mediate the generation of autophagy, so this study would like to explore whether ISKNV infected GF-1 cells will cause autophagy after the generation, and further explore the cell autophagy and virus expression, replication between the association. In the experimental results, it was found that viral infection could cause autophagy and inhibit the expression of viral and protein with UV treatment, autophagy inhibitor 3-MA, antioxidant such as NAC and AMPK inhibitor. It was found that the activity of reactive oxygen species induced by the decrease of viral replication decreased, and not only activity of AMPK increased but also the activity of mTOR decreased in the upstream molecules of autophagy, and the autophagy was found to be slowed down. It is known that viral infection can activate ROS to induce cell autophagy. The treatment of NAC with antioxidant is the most significant.

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