Reactive oxygen species (ROS) accumulation inside the cells instigates oxidative stress, activating stress-responsive genes. The viral strategies for promoting stressful conditions and utilizing the induced host proteins to enhance their replication remain elusive. The present work investigates the impact of oxidative stress responses on Newcastle disease virus (NDV) pathogenesis. Here, we show that the progression of NDV infection varies with intracellular ROS levels. Additionally, the results demonstrate that NDV infection modulates the expression of oxidative stress-responsive genes, majorly sirtuin 7 (SIRT7), a NAD+-dependent deacetylase. The modulation of SIRT7 protein, both through overexpression and knockdown, significantly impacts the replication dynamics of NDV in DF-1 cells. The activation of SIRT7 is found to be associated with the positive regulation of cellular protein deacetylation. Lastly, the results suggested that NDV-driven SIRT7 alters NAD+ metabolism in vitro and in ovo. We concluded that the elevated expression of NDV-mediated SIRT7 protein with enhanced activity metabolizes the NAD+ to deacetylase the host proteins, thus contributing to high virus replication.

中文翻译：

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新城疫病毒通过刺激氧化应激驱动的 Sirtuin 7 产生来调节其复制

细胞内活性氧（ROS）的积累会引发氧化应激，激活应激反应基因。促进应激条件和利用诱导的宿主蛋白增强其复制的病毒策略仍然难以捉摸。目前的工作研究氧化应激反应对新城疫病毒（NDV）发病机制的影响。在这里，我们发现 NDV 感染的进展随细胞内 ROS 水平的变化而变化。此外，结果表明NDV感染调节氧化应激反应基因的表达，主要是sirtuin 7 ( SIRT7 )，一种NAD +依赖性脱乙酰酶。SIRT7 蛋白的调节（通过过表达和敲低）显着影响 DF-1 细胞中 NDV 的复制动态。研究发现 SIRT7 的激活与细胞蛋白脱乙酰化的正向调节有关。最后，结果表明 NDV 驱动的 SIRT7 改变体外和卵内的NAD +代谢。我们得出的结论是，NDV 介导的 SIRT7 蛋白表达升高且活性增强，可代谢 NAD +使宿主蛋白脱乙酰化，从而促进病毒复制。