白點症病毒(white spot syndrome virus；WSSV)造成全球重大經濟損失，因此確定其發病機制將有相當的重要性。先前研究提出病毒基因體複製時期，誘發瓦氏效應及麩醯胺酸分解作用。麩醯胺酸分解作用有兩條路徑：α-KGDH介導的氧化路徑，以及IDH1或IDH2介導的還原途徑。本研究中指出白點症病毒基因體複製階段會增加α-KGDH及IDH1基因表現量，並提高還原性IDHs及氧化性α-KGDH酵素活性。以dsRNA分別使IDH1、IDH2及α-KGDH基因默化，得知三基因對白點症病毒的複製皆相當重要。利用[U-13C]麩醯胺酸以及[5-13C]麩醯胺酸作為穩定同位素標定(stable isotopic labeling)追蹤物，證實在病毒基因體複製階段，麩醯胺酸代謝的還原流顯著增加。再者，一系列的抑制試驗得知白點症病毒感染過程可能透過Ras參與活化麩醯胺酸分解作用。總而言之，病毒基因體複製階段相關酵素表現量被活化以增強麩醯胺酸代謝流，回補檸檬酸循環，而還原性麩醯胺酸分解路徑可能是主要產生脂質以支持白點症病毒在後期病毒顆粒的型態形成。

Although White spot syndrome virus (WSSV) has caused huge global economic losses, its pathogenesis remains poorly understood. We reported that WSSV triggered a Warburg effect, as well as glutaminolysis, at the WSSV genome replication stage. Glutamine metabolism occurs in two pathways: an α-KGDH-mediated oxidative pathway and an alternative reductive pathway, mediated by IDH1 or 2. Herein, we determined that gene expressions of α-KGDH and IDH1 were increased in WSSV-infected shrimp, with increased enzyme activity of α-KGDH and IDHs in the reductive pathway. Silencing α-KGDH, IDH1 and IDH2 with their respective dsRNAs implicated these three enzymes in WSSV replication. Moreover, at the replication stage, significant increases in amounts and production rates of metabolites in oxidative and reductive glutamine metabolic pathways were confirmed using [U-13C]glutamine and [5-13C]glutamine as tracers. In conclusion, at the viral genome replication stage, glutamine metabolic fluxes were increased, with elevated expression of related enzymes to replenish the TCA cycle and support WSSV morphogenesis.

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