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CCR4-NOT Complex 2-A Cofactor in Host Cell for Porcine Epidemic Diarrhea Virus Infection

文献类型： 外文期刊

作者： Wang, Jieru 1 ; Liu, Hailong 2 ; Yin, Dongdong 1 ; Zhou, Mei 1 ; Yin, Lei 1 ; Yang, Yuqing 2 ; Guo, Zishi 2 ; Shen, Xuehuai 1 ; Dai, Yin 1 ; Shi, Shaohua 1 ; Xie, Shengsong 2 ; Zhao, Ruihong 1 ; Zhou, Xueli 1 ; Hu, Xiaomiao 1 ; Hou, Hongyan 1 ; Wang, Chonglong 1 ; Pan, Xiaocheng 1 ;

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

2.Huazhong Agr Univ, Key Lab Agr Anim Genet Breeding & Reprod, Minist Educ, Wuhan 430070, Peoples R China

3.Huazhong Agr Univ, Key Lab Swine Genet & Breeding, Minist Agr & Rural Affairs, Wuhan 430070, Peoples R China

关键词： porcine epidemic diarrhea virus; CNOT2; surface plasmon resonance; interaction

期刊名称：GENES （ 影响因子：4.141； 五年影响因子：4.474 ）

ISSN：

年卷期： 2022 年 13 卷 9 期

页码：

收录情况： SCI

摘要： The porcine epidemic diarrhea virus (PEDV) has catastrophic impacts on the global pig industry. However, there is no consensus on the primary receptor associated with the PEDV invasion of host cells. An increasing number of studies have reported that PEDV invading host cells may require collaboration between multiple receptors and to better understand the virus-host interaction during PEDV entry, surface plasmon resonance (SPR) assays are performed to investigate relevant host factors interacting with PEDV spike-1 protein (S1) in Vero and IPEC-J2 cell membranes. Subsequently, the rabbit anti-PEDV S1 polyclonal antibody is used as bait to recognize the complexes of IPEC-J2 membrane proteins with or without PEDV infection, followed by detection using liquid chromatography with tandem mass spectrometry (LC-MS-MS). Our results show that 13 and 10 proteins interacting between the S1 protein and plasma membrane protein of Vero or IPEC-J2 can be identified. More specifically, a total of 11 differentially expressed interacting proteins were identified in IPEC-J2 membrane proteins after PEDV infection, compared to the uninfected group. Furthermore, we found that the differentially interacting protein CCR4-NOT complex 2 (CNOT2), identified in PEDV S1 with plasma membrane proteins of Vero cells, is involved in viral infection. The results show that the knockout of CNOT2 significantly inhibits PEDV replication in vitro. These data provide novel insights into the entry mechanism of PEDV.

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