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伪狂犬病毒操纵线粒体色氨酰-tRNA 合成酶 2 进行病毒复制。

Pseudorabies virus manipulates mitochondrial tryptophanyl-tRNA synthetase 2 for viral replication.

机构信息

College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China; Key Laboratory of Animal Biochemistry and Nutrition, Ministry of Agriculture and Rural Affairs, Zhengzhou 450046, China; Key Laboratory of Veterinary Biotechnology of Henan Province, Henan Agricultural University, Zhengzhou 450046, China.

School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.

出版信息

Virol Sin. 2024 Jun;39(3):403-413. doi: 10.1016/j.virs.2024.04.003. Epub 2024 Apr 16.

Abstract

The pseudorabies virus (PRV) is identified as a double-helical DNA virus responsible for causing Aujeszky's disease, which results in considerable economic impacts globally. The enzyme tryptophanyl-tRNA synthetase 2 (WARS2), a mitochondrial protein involved in protein synthesis, is recognized for its broad expression and vital role in the translation process. The findings of our study showed an increase in both mRNA and protein levels of WARS2 following PRV infection in both cell cultures and animal models. Suppressing WARS2 expression via RNA interference in PK-15 ​cells led to a reduction in PRV infection rates, whereas enhancing WARS2 expression resulted in increased infection rates. Furthermore, the activation of WARS2 in response to PRV was found to be reliant on the cGAS/STING/TBK1/IRF3 signaling pathway and the interferon-alpha receptor-1, highlighting its regulation via the type I interferon signaling pathway. Further analysis revealed that reducing WARS2 levels hindered PRV's ability to promote protein and lipid synthesis. Our research provides novel evidence that WARS2 facilitates PRV infection through its management of protein and lipid levels, presenting new avenues for developing preventative and therapeutic measures against PRV infections.

摘要

伪狂犬病毒(PRV)被鉴定为一种双链 DNA 病毒,可引起疱疹病毒脑炎,在全球范围内造成重大经济影响。参与蛋白质合成的线粒体蛋白色氨酰-tRNA 合成酶 2(WARS2)因广谱表达和在翻译过程中的重要作用而受到关注。我们的研究发现,在细胞培养和动物模型中,PRV 感染后 WARS2 的 mRNA 和蛋白水平均增加。在 PK-15 细胞中通过 RNA 干扰抑制 WARS2 表达可降低 PRV 感染率,而增强 WARS2 表达则导致感染率增加。此外,发现 WARS2 对 PRV 的激活依赖于 cGAS/STING/TBK1/IRF3 信号通路和干扰素-α受体-1,这表明它通过 I 型干扰素信号通路进行调节。进一步分析表明,降低 WARS2 水平可阻碍 PRV 促进蛋白质和脂质合成的能力。我们的研究提供了新的证据,表明 WARS2 通过调节蛋白质和脂质水平促进 PRV 感染,为开发针对 PRV 感染的预防和治疗措施提供了新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6681/11279775/f82046e45747/gr1.jpg

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