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Effect of heat shock on murine norovirus replication in RAW264.7 cells.

Authors
  • Ma, Chang1
  • Zhang, Xuliang1
  • You, Jinwei1
  • Dong, Min1
  • Yun, Shifeng2
  • Liu, Jie3
  • 1 Department of Comparative Medicine, Jinling Hospital, Nanjing, PR China. , (China)
  • 2 Department of Comparative Medicine, Jinling Hospital, Nanjing, PR China; Clinical School of Medical College of Nanjing University, Nanjing, PR China. Electronic address: [email protected] , (China)
  • 3 Department of Comparative Medicine, Jinling Hospital, Nanjing, PR China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Microbial Pathogenesis
Publisher
Elsevier
Publication Date
Feb 26, 2020
Volume
142
Pages
104102–104102
Identifiers
DOI: 10.1016/j.micpath.2020.104102
PMID: 32112809
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Murine norovirus (MNV), is a prevalent pathogen of laboratory mice closely related to human norovirus (HuNoV), a contagious pathogen known to cause gastroenteritis worldwide; however, the mechanism of norovirus replication remains poorly understood. Both heat shock protein 90 (Hsp90) and heat shock protein 70 (Hsp70) play an important role in viral genome replication and viral gene expression. In this study, we first found that heat stress exerted a positive effect on the replication of MNV in the murine macrophage RAW264.7 cell line. Inhibition of Hsp70 and Hsp90 by the specific inhibitors, KNK437 and 17-AGG, respectively showed that Hsp70 and Hsp90 enhanced MNV genome replication and virion production. In addition, we found that KNK437 and 17-AGG could decrease the level of IL-1β, IL-10, and TNF-α mRNA expression in MNV-infected cells. These data suggested that heat stress can positively regulate MNV replication, which advances our understanding of the molecular mechanism of MNV infection. Copyright © 2020 Elsevier Ltd. All rights reserved.

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