Infectious Spleen and Kidney Necrosis Virus ORF093R and ORF102R Regulate Glutamate Metabolic Reprogramming to Support Virus Proliferation by Interacting with c-Myc
文献类型： 外文期刊
作者： Niu, Yinjie 1 ; Ye, Caimei 1 ; Lin, Qiang 1 ; Liang, Hongru 1 ; Luo, Xia 1 ; Ma, Baofu 1 ; Li, Ningqiu 1 ; Fu, Xiaozhe 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Key Lab Aquat Anim Immune Technol, Key Lab fishery Drug Dev,Minist Agr Rural Affairs, Guangzhou 510380, Peoples R China
关键词： ISKNV; c-Myc; glutamine metabolism
期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：4.9； 五年影响因子：5.7 ）
ISSN： 1661-6596
年卷期： 2025 年 26 卷 2 期
页码：
收录情况： SCI
摘要： Glutamine metabolism is essential for infectious spleen and kidney necrosis virus (ISKNV) replication. Glutaminase 1 (GLS1), the key enzyme of the glutamine metabolism, and c-Myc positively regulate ISKNV infection, while c-Myc is closely correlated with GLS1. However, the regulatory mechanism among ISKNV, c-Myc and glutamine metabolism remains unclear. Here, we indicated that c-Myc increased glutamine uptake by increasing the GLS1, glutamate dehydrogenase (GDH) and isocitrate dehydrogenase (IDH2) expression of glutamine metabolism. ISKNV ORF102R, ORF093R and ORF118L co-located with c-Myc in CPB cells. Co-IP results showed that ISKNV ORF102R and ORF093R interacted with c-Myc, while ORF118L did not interact with c-Myc. The expression levels of c-Myc, GLS1 and IDH2 were increased in ISKNV ORF093R expression cells, and the mRNA and protein levels of GLS1 were upregulated in ISKNV 102R-expressing cells. These results indicated that ISKNV reconstructed glutamine metabolism to satisfy the energy and macromolecule requirements for virus proliferation by ORF093R and ORF102R interacting with c-Myc, which provides the foundation for innovative antiviral strategies.
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