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Host protein PRPS2 interact with the non-structural protein p17 of Avian Reovirus and promote viral replication

文献类型： 外文期刊

作者： Hu, Xiaomiao 1 ; Zhao, Ruihong 1 ; Li, Wei 2 ; Pan, Xiaocheng 1 ; Dai, Yin 1 ; Wu, Huimin 3 ; Wu, Yantao 3 ; Zhang, Chengcheng 3 ;

作者机构： 1.Anhui Acad Agr Sci, Inst Anim Husb & Vet Med, Livestock & Poultry Epidem Dis Res Ctr Anhui Prov, Anhui Prov Key Lab Livestock & Poultry Prod Safety, Hefei 230031, Anhui, Peoples R China

2.Yangzhou Polytech Coll, Yangzhou 225009, Peoples R China

3.Yangzhou Univ, Coll Vet Med, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China

关键词： Avian reovirus; p17 protein; PRPS2; Replication

期刊名称：POULTRY SCIENCE （ 影响因子：4.2； 五年影响因子：4.5 ）

ISSN： 0032-5791

年卷期： 2025 年 104 卷 1 期

页码：

收录情况： SCI

摘要： Avian reovirus (ARV) is highly prevalent in healthy poultry flocks and has been linked to viral arthritis/ tendonitis, dwarf syndrome, chronic respiratory disease, and immunosuppression in avian species, resulting in significant economic losses within the poultry industry. The non-structural protein p17 encoded by ARV induces cellular autophagy and facilitates viral proliferation, playing a pivotal role in viral pathogenesis. To further elucidate the pathogenic mechanism basis of ARV p17 protein function, we employed a yeast two-hybrid system to identify Phosphoribosyl pyrophosphate synthetase 2 (PRPS2) as an interacting host protein with p17. In this study, we validated the interaction between PRPS2 and p17 using laser confocal microscopy, coimmunoprecipitation, and GST-Pulldown assays. Moreover, our findings demonstrate that the C-terminal region of PRPS2 is responsible for its binding to the p17 protein. Intriguingly, ARV infection significantly upregulated PRPS2 expression levels. Additionally, PRPS2 was shown to have a substantial impact on ARV replication; overexpression of PRPS2 increased ARV replication while knockdown of PRPS2 resulted in decreased quantities of ARV particles. Furthermore, our findings suggest that this process involves cellular apoptosis as a potential mechanism underlying these observations. Overall, this research provides valuable insights into elucidating the function of the p17 protein and sheds light on the pathogenic mechanism involving ARV-induced cellular apoptosis while offering novel perspectives for exploring therapeutic targets against ARV.

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