Department of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Research Organization for Nano and Life Innovations, Waseda University, Tokyo, Japan.
Commun Biol. 2023 May 20;6(1):546. doi: 10.1038/s42003-023-04924-w.
In addition to the Warburg effect, which increases the availability of energy and biosynthetic building blocks in WSSV-infected shrimp, WSSV also induces both lipolysis at the viral genome replication stage (12 hpi) to provide material and energy for the virus replication, and lipogenesis at the viral late stage (24 hpi) to complete virus morphogenesis by supplying particular species of long-chain fatty acids (LCFAs). Here, we further show that WSSV causes a reduction in lipid droplets (LDs) in hemocytes at the viral genome replication stage, and an increase in LDs in the nuclei of WSSV-infected hemocytes at the viral late stage. In the hepatopancreas, lipolysis is triggered by WSSV infection, and this leads to fatty acids being released into the hemolymph. β-oxidation inhibition experiment reveals that the fatty acids generated by WSSV-induced lipolysis can be diverted into β-oxidation for energy production. At the viral late stage, WSSV infection leads to lipogenesis in both the stomach and hepatopancreas, suggesting that fatty acids are in high demand at this stage for virion morphogenesis. Our results demonstrate that WSSV modulates lipid metabolism specifically at different stages to facilitate its replication.
除了沃伯格效应（Warburg effect）增加了 WSSV 感染虾中能量和生物合成构建块的可用性之外，WSSV 还在病毒基因组复制阶段（12 hpi）诱导脂解，为病毒复制提供物质和能量，在病毒晚期（24 hpi）诱导脂肪生成，通过提供特定种类的长链脂肪酸（LCFAs）来完成病毒形态发生。在这里，我们进一步表明，WSSV 在病毒基因组复制阶段导致血细胞中的脂滴（LDs）减少，而在病毒晚期感染血细胞的细胞核中 LDs 增加。在肝胰腺中，WSSV 感染触发脂解，导致脂肪酸释放到血淋巴中。β-氧化抑制实验表明，WSSV 诱导的脂解产生的脂肪酸可以被转移到β-氧化中以产生能量。在病毒晚期，WSSV 感染导致胃和肝胰腺中的脂肪生成，表明在此阶段病毒形态发生需要大量脂肪酸。我们的结果表明，WSSV 在不同阶段特异性地调节脂质代谢，以促进其复制。
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