Mortalin restricts porcine epidemic diarrhea virus entry by downregulating clathrin-mediated endocytosis
文献类型: 外文期刊
作者: Fan, Baochao 1 ; Zhu, Lin 1 ; Chang, Xinjian 1 ; Zhou, Jinzhu 1 ; Guo, Rongli 1 ; Zhao, Yongxiang 1 ; Shi, Danyi 1 ; Niu, 1 ;
作者机构: 1.Minist Agr, Inst Vet Med, Jiangsu Acad Agr Sci, Key Lab Vet Biol Engn & Technol, Nanjing 210014, Jiangsu, Peoples R China
2.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225000, Jiangsu, Peoples R China
3.Minist Sci & Technol, Jiangsu Key Lab Food Qual & Safety, State Key Lab Cultivat Base, Nanjing 210014, Jiangsu, Peoples R China
4.Huaiyin Inst Technol, Jiangsu Prov Key Construct Lab Probiot Preparat, Huaian 223003, Peoples R China
5.Hebei Normal Univ Sci & Technol, Coll Anim Sci & Technol, Qinhuangdao 066004, Hebei, Peoples R China
6.Nanjing Agr Univ, Coll Vet Med, 1 Wei Gang, Nanjing 210095, Jiangsu, Peoples R China
7.Jiangsu Univ, Sch Food & Biol Engn, Zhenjiang 212013, Jiangsu, Peoples R China
8.Washington Univ, Dept Mol Microbiol, St Louis, MO 63110 USA
关键词: Mortalin; PEDV; CLTC; Clathrin-mediated endocytosis
期刊名称:VETERINARY MICROBIOLOGY ( 影响因子:3.293; 五年影响因子:3.599 )
ISSN: 0378-1135
年卷期: 2019 年 239 卷
页码:
收录情况: SCI
摘要: Clathrin-mediated endocytosis is a mechanism used for the invasion of cells by a variety of viruses. Mortalin protein is involved in a variety of cellular functions and plays a role in viral infection. In this study, we found that mortalin significantly inhibited the replication of porcine epidemic diarrhea virus (PEDV) through restricting virus entry. Mechanistically, a biochemical interaction between the carboxyl terminus of mortalin and clathrin heavy chain (CLTC) was been found, and mortalin could induce CLTC degradation through the proteasomal pathway, thereby inhibiting the clathrin-mediated endocytosis of PEDV into host cells. In addition, artificial changes in mortalin expression affected the cell entry of transferrin, further confirming the above results. Finally, we confirmed that this host-mounted antiviral mechanism was broadly applicable to other viruses, such as vesicular stomatitis virus (VSV), rotavirus (RV), and transmissible gastroenteritis virus (TGEV), which use the same clathrin-mediated endocytic to entry. These results reveal a new function of mortalin in inhibiting endocytosis, and provide a novel strategy for treating PEDV infections.
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