Porcine Epidemic Diarrhea Virus Infection Subverts Arsenite-Induced Stress Granules Formation
文献类型: 外文期刊
作者: Guo, Xiaozhen 1 ; Yu, Kejian 2 ; Xin, Zhonghao 2 ; Liu, Liping 1 ; Gao, Yuehua 1 ; Hu, Feng 1 ; Ma, Xiuli 1 ; Yu, Kexiang 1 ; Li, Yufeng 1 ; Huang, Bing 1 ; Yan, Zhengui 2 ; Wu, Jiaqiang 2 ;
作者机构: 1.Shandong Acad Agr Sci, Inst Poultry Sci, Shandong Key Lab Immun & Diag Poultry Dis, Jinan, Peoples R China
2.Shandong Agr Univ, Coll Anim Sci & Technol, Shandong Prov Key Lab Anim Biotechnol & Dis Contro, Tai An, Peoples R China
3.Shandong Acad Agr Sci, Inst Anim Sci & Vet Med, Shandong Key Lab Dis Control & Breeding, Jinan, Peoples R China
4.Shandong Normal Univ, Coll Life Sci, Shandong Key Lab Anim Resistant Biol, Jinan, Peoples R China
关键词: PEDV replication; stress granules; sodium arsenite; papain-like protease; interaction mechanism
期刊名称:FRONTIERS IN MICROBIOLOGY ( 影响因子:6.064; 五年影响因子:6.843 )
ISSN:
年卷期: 2022 年 13 卷
页码:
收录情况: SCI
摘要: 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.
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