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

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.
AuthorsBaochao 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
JournalVeterinary microbiology (Vet Microbiol) Vol. 239 Pg. 108455 (Dec 2019) ISSN: 1873-2542 [Electronic] Netherlands
PMID31767073 (Publication Type: Journal Article)
CopyrightCopyright © 2019 Elsevier B.V. All rights reserved.
Chemical References
  • Clathrin
  • HSP70 Heat-Shock Proteins
  • RNA, Small Interfering
  • mortalin
Topics
  • Animals
  • Cell Line
  • Chlorocebus aethiops
  • Clathrin (metabolism)
  • Down-Regulation (physiology)
  • Endocytosis (physiology)
  • Gene Silencing
  • HSP70 Heat-Shock Proteins (genetics, metabolism)
  • HeLa Cells
  • Host Microbial Interactions (physiology)
  • Humans
  • Porcine epidemic diarrhea virus (physiology)
  • RNA, Small Interfering (metabolism)
  • Vero Cells
  • Virus Internalization
  • Virus Replication (physiology)

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