FUBP3 Degrades the Porcine Epidemic Diarrhea Virus Nucleocapsid Protein and Induces the Production of Type I Interferon
Sujie Dong, Ning Kong, Chunmei Wang, Youwen Li, Dage Sun, Wenzhen Qin, Huanjie Zhai, Xueying Zhai, Xinyu Yang, Chenqian Ye, Manqing Ye, Changlong Liu, Lingxue Yu, Hao Zheng, Tong Wu, Hai Yu, Wen Zhang, Guangzhi Tong, Tongling Shan
Abstract
PEDV refers to the alphacoronavirus that is found globally and has re-emerged recently, causing severe financial losses. In PEDV infection, the host activates various host restriction factors to maintain innate antiviral responses to suppress virus replication. Here, FUBP3 was detected as a new host restriction factor. FUBP3 was found to suppress PEDV replication via the degradation of the PEDV-encoded nucleocapsid (N) protein via E3 ubiquitin ligase MARCH8 as well as the cargo receptor NDP52/CALCOCO2. Additionally, FUBP3 upregulated the IFN-I signaling pathway by interacting with and increasing tumor necrosis factor (TNF) receptor-associated factor 3 (TRAF3) expression. This study further demonstrated that another layer of complexity could be added to the selective autophagy and innate immune response against PEDV infection are complicated.