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Accelerated Metabolite Levels of Aerobic Glycolysis and the Pentose Phosphate Pathway Are Required for Efficient Replication of Infectious Spleen and Kidney Necrosis Virus in Chinese Perch Brain Cells

文献类型： 外文期刊

作者： Guo, Xixi 1 ; Wu, Shiwei 1 ; Li, Ningqiu 1 ; Lin, Qiang 1 ; Liu, Lihui 1 ; Liang, Hongru 1 ; Niu, Yinjie 1 ; Huang, Zhibi 1 ;

作者机构： 1.Chinese Acad Fishery Sci, Key Lab Fishery Drug Dev, Key Lab Aquat Anim Immune Technol, Minist Agr & Rural Affairs,Pearl River Fisheries, Guangzhou 510380, Guangdong, Peoples R China

2.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai 201306, Peoples R China

关键词： ISKNV; Siniperca chuatsi; glucose metabolism reprogramming; aerobic glycolysis; pentose phosphate pathway (PPP); TCA cycle

期刊名称：BIOMOLECULES （ 影响因子：4.879； 五年影响因子：5.362 ）

ISSN：

年卷期： 2019 年 9 卷 9 期

页码：

收录情况： SCI

摘要： Glucose is a main carbon and energy source for virus proliferation and is usually involved in the glycolysis, pentose phosphate pathway (PPP), and tricarboxylic acid cycle (TCA cycle) pathways. In this study, we investigated the roles of glucose-related metabolic pathways during the replication of infectious spleen and kidney necrosis virus (ISKNV), which has caused serious economic losses in the cultured Chinese perch (Siniperca chuatsi) industry. We found that ISKNV infection enhanced the metabolic pathways of the PPP and the TCA cycle at the early stage of the ISKNV infection cycle and enhanced the glycolysis pathway at the late stage of the ISKNV infection cycle though the comprehensive analysis of transcriptomics, proteomics, and metabolomics. The advanced results proved that ISKNV replication induced upregulation of aerobic glycolysis at the late stage of ISKNV infection cycle and aerobic glycolysis were required for ISKNV multiplication. In addition, the PPP, providing nucleotide biosynthesis, was also required for ISKNV multiplication. However, the TCA cycle involving glucose was not important and necessary for ISKNV multiplication. The results reported here provide new insights into viral pathogenesis mechanism of metabolic shift, as well as antiviral treatment strategies.

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