4.6 Article

Porcine Epidemic Diarrhea Virus Infection Subverts Arsenite-Induced Stress Granules Formation

期刊

FRONTIERS IN MICROBIOLOGY
卷 13, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2022.931922

关键词

PEDV replication; stress granules; sodium arsenite; papain-like protease; interaction mechanism

资金

  1. Shandong Provincial Natural Science Foundation Youth Project [ZR2021QC054]
  2. Shandong Provincial Modern Agricultural Industry and Technology System [SDAIT-08-01]
  3. Great Scientific and Technological Innovation Projects in Shandong Province [2020CXGC010801]
  4. Shandong Key Provincial Research and Development Program [2019GNC106044]
  5. National Natural Science Funds [32070178, 32002286]
  6. Agricultural Scientific and Technological Innovation Project of Shandong Academy of Agricultural Sciences [CXGC2021A12, CXGC2021A39]

向作者/读者索取更多资源

This study found that PEDV-infected cells contain SGs and are resistant to SA-induced SGs formation. PEDV infection disrupts SGs formation by downregulating G3BP1 expression. PEDV replication is significantly enhanced when SGs assembly is impaired by silencing G3BP1.
Stress granules (SGs) are dynamic cytoplasmic protein-RNA structures that form in response to various stress conditions, including viral infection. Porcine epidemic diarrhea virus (PEDV) variant-related diarrhea has caused devastating economic losses to the swine industry worldwide. In this study, we found that the percentage of PEDV-infected cells containing SGs is nearly 20%; meanwhile, PEDV-infected cells were resistant to sodium arsenite (SA)-induced SGs formation, as demonstrated by the recruitment of SGs marker proteins, including G3BP1 and TIA1. Moreover, the formation of SGs induced by SA treatment was suppressed by PEDV papain-like protease confirmed by confocal microscopy. Further study showed that PEDV infection disrupted SGs formation by downregulating G3BP1 expression. Additionally, PEDV replication was significantly enhanced when SGs' assembly was impaired by silencing G3BP1. Taken together, our findings attempt to illuminate the specific interaction mechanism between SGs and PEDV, which will help us to elucidate the pathogenesis of PEDV infection in the near future.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据