HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >

Necroptosis of neuronal cells is related to the neuropathology of tick-borne encephalitis

This item is licensed under:Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International

Files in This Item:
Supplementary materials for TBEV necroptosis.docxSupplementary materials25.71 kBMicrosoft Word XMLView/Open
TBEV necroptosis 3rd clear version.pdf1.72 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/90730

Title: Necroptosis of neuronal cells is related to the neuropathology of tick-borne encephalitis
Authors: Tsujino, Dai Browse this author
Yoshii, Kentaro Browse this author
Kajiyama, Misa Browse this author
Takahashi, Yuji Browse this author
Maekawa, Naoya Browse this author
Kariwa, Hiroaki Browse this author →KAKEN DB
Kobayashi, Shintaro Browse this author →KAKEN DB
Keywords: Tick-borne encephalitis virus
Programmed cell death
Necroptosis
Issue Date: Nov-2022
Publisher: Elsevier
Journal Title: Virus Research
Volume: 321
Start Page: 198914
Publisher DOI: 10.1016/j.virusres.2022.198914
Abstract: Tick-borne encephalitis virus (TBEV) is a zoonotic virus that causes tick-borne encephalitis (TBE) in humans. Infections of Sapporo-17-Io1 (Sapporo) and Oshima 5-10 (Oshima) TBEV strains showed different pathogenic effects in mice. However, the differences between the two strains are unknown. In this study, we examined neuronal degeneration and death, and activation of glial cells in mice inoculated with each strain to investigate the pathogenesis of TBE. Viral growth was similar between Sapporo and Oshima, but neuronal degeneration and death, and activation of glial cells, was more prominent with Oshima. In human neuroblastoma cells, apoptosis and pyroptosis were not observed after TBEV infection. However, the expression of the necroptosis marker, mixed lineage kinase domain-like (MLKL) protein, was upregulated by TBEV infection, and this upregulation was more pronounced in Oshima than Sapporo infections. As necroptosis is a pro-inflammatory type of cell death, differences in necroptosis induction might be involved in the differences in neuropathogenicity of TBE.
Rights: © 2022. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/90730
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小林 進太郎

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 

 - Hokkaido University