背景回顾：The plant antioxidant system plays important roles in response to diverse abiotic and biotic stresses. 

提出问题：However, the effects of virus infection on host redox homeostasis and how antioxidant defense pathway is manipulated by viruses remain poorly understood. 

研究基础：We previously demonstrated that the Barley stripe mosaic virus (BSMV) γb protein is recruited to the chloroplast by the viral αa replicase to enhance viral replication. 

主要发现：Here, we show that BSMV infection induces chloroplast oxidative stress.

γb蛋白与NTRC：The versatile γb protein interacts directly with NADPH-dependent thioredoxin reductase C (NTRC), a core component of chloroplast antioxidant systems. 

结果2-NTRC过表达和干扰表达：Overexpression of NbNTRC significantly impairs BSMV replication in Nicotiana benthamiana plants, whereas disruption of NbNTRC expression leads to increased viral accumulation and infection severity. 

结果3-γb蛋白作用机制：To counter NTRC-mediated defenses, BSMV employs the γb protein to competitively interfere with NbNTRC binding to 2-Cys Prx. 

结论：Altogether, this study indicates that beyond acting as a helicase enhancer, γb also subverts NTRC-mediated chloroplast antioxidant defenses to create an oxidative microenvironment conducive to viral replication.

 摘 要 

植物抗氧化系统在响应各种非生物和生物胁迫方面发挥着重要作用。然而，病毒感染对寄主植物体内氧化还原稳态的影响以及病毒如何控制植物抗氧化防御途径仍不清楚。作者在之前的研究中发现，大麦条纹花叶病毒（BSMV）γb蛋白会被病毒的αa复制酶招募到叶绿体，以增强病毒复制。本文中，作者发现BSMV侵染植物会诱导植物叶绿体的氧化胁迫。多功能γb蛋白能够直接与NADPH依赖的硫氧还蛋白还原酶C（NTRC）相互作用，而NTRC是叶绿体抗氧化系统的核心组成成分。NbNTRC的过度表达显著抑制了烟草植株中BSMV的复制，而NbNTRC表达的破坏会导致病毒积累和感染严重程度的增加。为了对抗植物中NTRC介导的防御，BSMV利用γb蛋白竞争性地干扰NbNTRC与2-Cys-Prx的结合。综上，本文的研究结果表明，BSMV的γb蛋白除了作为解旋酶增强子外，还能够破坏植物中NTRC介导的叶绿体抗氧化防御，以创造有利于病毒复制的氧化微环境。