Encephalomyocarditis virus impairs the blood-brain barrier by degrading tight junction proteins via AKT3-dependent autophagic and apoptotic pathways.
Overview
- Engineering Research Center of Key Technology and Industrialization of Cell-Based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou, China
- Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou, China
- Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou, China
- School of Bioengineering, Northwest Minzu University, Lanzhou, China
- College of Life Science and Engineering, Northwest Minzu University, Lanzhou, China
- Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, Australia
Abstract
Encephalomyocarditis virus (EMCV) infection causes viral encephalitis; however, the mechanisms underlying blood-brain barrier (BBB) disruption remain poorly understood. Here, we demonstrate that EMCV actively replicates in mouse brain tissue, induces robust neuroinflammation characterized by elevated proinflammatory cytokines and chemokines, and markedly increases BBB permeability as evidenced by Evans blue and sodium fluorescein extravasation. Importantly, tight junction (TJ) proteins ZO-1 and Occludin are selectively degraded at the post-transcriptional level, whereas Claudin-5 expression remains stable. Consistently, in vitro BBB models confirmed EMCV traversal, reduced transendothelial electrical resistance, and TJ disruption. Mechanistically, EMCV induces biphasic PI3K/
Reproduced under the paper's license (CC BY-NC), from the paper cited above.
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Data
Datasets cited
- figshare:30984970, at figshare; found in “Data availability statement”
Data availability statement
The data that support the findings of this study are openly available in figshare (https://
Reproduced under the paper's license (CC BY-NC), from the paper cited above.
Versions
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Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 12 authors, 6 keywords, 12 MeSH terms, 5 funders, 76 references.
Cite
This paper
Dou, X., Wang, N., Yao, S., Chen, X., Li, S., Xie, J., Li, X., Yang, Y., Wen, Y., Idris, A., Li, H., & Feng, R. (2026). Encephalomyocarditis virus impairs the blood-brain barrier by degrading tight junction proteins via AKT3-dependent autophagic and apoptotic pathways. Virulence, 17(1), 2697518. https://
BibTeX
@article{dou2026encephal
author = {Dou, Xueer and Wang, Na and Yao, Shuangshuang and Chen, Xinrui and Li, Shasha and Xie, Jingying and Li, Xiangrong and Yang, Yanmei and Wen, Yanqiao and Idris, Adi and Li, Huixia and Feng, Ruofei},
title = {{Encephalomyocarditis virus impairs the blood-brain barrier by degrading tight junction proteins via AKT3-dependent autophagic and apoptotic pathways}},
journal = {Virulence},
year = {2026},
month = jul,
volume = {17},
number = {1},
pages = {2697518},
publisher = {Taylor \& Francis},
issn = {2150-5594},
doi = {10.1080/
url = {https://
pmid = {42397844},
pmcid = {PMC13336293}
}
RIS
TY - JOUR
AU - Dou, Xueer
AU - Wang, Na
AU - Yao, Shuangshuang
AU - Chen, Xinrui
AU - Li, Shasha
AU - Xie, Jingying
AU - Li, Xiangrong
AU - Yang, Yanmei
AU - Wen, Yanqiao
AU - Idris, Adi
AU - Li, Huixia
AU - Feng, Ruofei
TI - Encephalomyocarditis virus impairs the blood-brain barrier by degrading tight junction proteins via AKT3-dependent autophagic and apoptotic pathways
T2 - Virulence
J2 - Virulence
PY - 2026
DA - 2026/
VL - 17
IS - 1
SP - 2697518
SN - 2150-5594
PB - Taylor & Francis
DO - 10.1080/
UR - https://
LA - en
ER -
CSL-JSON
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