Mortalin restricts porcine epidemic diarrhea virus entry by downregulating clathrin-mediated endocytosis

Baochao Fan, Lin Zhu, Xinjian Chang, Jinzhu Zhou, Rongli Guo, Yongxiang Zhao, Danyi Shi, Beibei Niu, Jun Gu, Zhengyu Yu, Tao Song, Chuping Luo, Zengjun Ma, Juan Bai, Bin Zhou, Siyuan Ding, Kongwang He, Bin Li

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

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.

Original languageEnglish
Article number108455
JournalVeterinary Microbiology
Volume239
DOIs
StatePublished - Dec 2019

Keywords

  • CLTC
  • Clathrin-mediated endocytosis
  • Mortalin
  • PEDV

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