BTG3 inhibits porcine epidemic diarrhea virus replication by promoting viral S2 protein degradation through the autophagy and proteasome pathways
文献类型： 外文期刊
作者： Zhu, Qingxiao 1 ; Liu, Tian 3 ; Qin, Wenzhen 3 ; Yang, Xinyu 3 ; Tong, Wu 3 ; Yu, Hai 3 ; Zheng, Hao 3 ; Tong, Guangzhi 3 ; Shan, Tongling 3 ; Zhang, Yu 5 ; Liu, Xuelan 1 ; Kong, Ning 2 ;
作者机构： 1.Anhui Agr Univ, Coll Vet Med, Anim Derived Food Safety Innovat Team, Hefei 230036, Peoples R China
2.Shanghai Key Lab Vet & Biotechnol, Shanghai 200240, Peoples R China
3.Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China
4.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Peoples R China
5.Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Sch Med, Dept Prevent Dent,Coll Stomatol, Shanghai, Peoples R China
关键词： BTG3; PEDV S2 subunit; Degradation; Autophagy pathway
期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：2.7； 五年影响因子：2.9 ）
ISSN： 0378-1135
年卷期： 2025 年 302 卷
页码：
收录情况： SCI
摘要： BTG3, which belongs to the BTG/Tob gene family, is involved in various physiological processes. Infection with porcine epidemic diarrhea virus (PEDV), an alphacoronavirus, is associated with high mortality rates among piglets, contributing to major economic losses. This study elucidated a novel mechanism through which BTG3 suppresses PEDV replication. Endogenous BTG3 protein expression was upregulated in PEDV-infected host cells. PEDV replication was suppressed upon BTG3 overexpression but enhanced upon BTG3 knockdown. Additionally, BTG3 inhibited viral proliferation by targeting and degrading the S2 subunit of the PEDV spike (S) protein through both autophagy and proteasome pathways. BTG3 interacted and co-localized with the S2 protein, promoting S2 protein degradation through the recruitment of the cargo receptor NDP52 and the E3 ubiquitin ligase MARCHF8. In summary, this study elucidated a novel antiviral mechanism in which the host BTG3 targeted the viral S2 protein to inhibit PEDV proliferation through autophagy and proteasome pathways. These findings indicate that BTG3 is a potential novel target for the prevention and control of PEDV.
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