Role of lipid metabolism in white spot syndrome virus replication

• Main Authors: Cheng-ShunCheng, 鄭丞舜
• Other Authors: Han-Ching Wang
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/bn268b

碩士 === 國立成功大學 === 生物科技研究所 === 104 === 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.