He Honghui, Yuan Kai, Pan Junming, Weng Shaoping, Li Chaozheng, Chen Yihong, He Jianguo
State Key Laboratory of Biocontrol, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, 510275, China.
School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, 510275, China.
Adv Sci (Weinh). 2025 May;12(18):e2407695. doi: 10.1002/advs.202407695. Epub 2025 Mar 16.
Reactive oxygen species (ROS) of hosts are widely involved in intracellular signaling and against pathogens. Viruses manipulate ROS homeostasis of hosts as a strategy to evade ROS-mediated negative effects of their infection, but the mechanisms remain unclear. The economically important aquaculture shrimp, Litopenaeus vannamei, is selected to investigate the molecular mechanism of how white spot syndrome virus (WSSV) regulates ROS dynamics and enhances viral replication. WSSV protein wsv220 binds to the repressor of shrimp nuclear factor erythroid 2-related factor 2 (LvNrf2), called Kelch-like ECH-associated protein 1 (LvKeap1), disrupting LvNrf2/LvKeap1 complex and facilitating LvNrf2 nuclear translocation. This activation of LvNrf2 causes up-regulation of antioxidant genes, including glucose-6-phosphate dehydrogenase (LvG6PDH), which increases nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH) production, effectively eliminating excessive ROS. Moreover, WSSV exploits LvNrf2 to establish a positive feedback loop by up-regulating viral immediate early gene wsv051, which further enhances wsv220 expression. Knockdown of LvNrf2 or LvG6PDH reduces WSSV replication and increases host ROS levels. Therefore, WSSV hijacks LvNrf2 pathway to maintain ROS homeostasis and establishes a positive feedback loop to facilitate WSSV replication. These findings reveal a novel molecular mechanism of viral manipulation of host ROS dynamics and suggest potential antiviral strategies targeting LvNrf2 pathway.
宿主的活性氧(ROS)广泛参与细胞内信号传导并对抗病原体。病毒操纵宿主的ROS稳态,以此作为逃避ROS介导的感染负面影响的策略,但其机制尚不清楚。本研究选取具有重要经济价值的养殖对虾凡纳滨对虾,以探究白斑综合征病毒(WSSV)调节ROS动态并增强病毒复制的分子机制。WSSV蛋白wsv220与虾核因子红细胞2相关因子2(LvNrf2)的抑制因子(即kelch样ECH相关蛋白1,LvKeap1)结合,破坏LvNrf2/LvKeap1复合物,促进LvNrf2核转位。LvNrf2的这种激活导致抗氧化基因上调,包括葡萄糖-6-磷酸脱氢酶(LvG6PDH),从而增加烟酰胺腺嘌呤二核苷酸磷酸(NADPH)和谷胱甘肽(GSH)的产生,有效清除过量的ROS。此外,WSSV利用LvNrf2通过上调病毒立即早期基因wsv051建立正反馈回路,进而增强wsv220的表达。敲低LvNrf2或LvG6PDH可降低WSSV复制并提高宿主机体ROS水平。因此,WSSV劫持LvNrf2途径以维持ROS稳态,并建立正反馈回路以促进WSSV复制。这些发现揭示了病毒操纵宿主ROS动态的一种新分子机制,并提出了针对LvNrf2途径的潜在抗病毒策略。