The host cells suppress the proliferation of pseudorabies virus by regulating the PI3K/Akt/mTOR pathway

PRV, known for its neurotropic properties, is capable of inducing severe neuronal damage. Our study discovered that following PRV infection, the expression of MMP2 was upregulated, leading to the degradation of ZO-1. Furthermore, upon PRV infection in the host, the promoter of TIMP1 is significantly activated, resulting in a significant increase in TIMP1 protein levels. This upregulation of TIMP1 inhibits the proliferation of PRV through the PI3K/Akt signaling pathway. This study elucidated the mechanism through which PRV, including the PRV XJ delgE/gI/TK strains, compromises the blood-brain barrier and identifies the antiviral response characterized by the activation of the PI3K/Akt signaling pathway within infected host cells. These findings provide potential therapeutic targets for the clinical management and treatment of PRV.

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Publication Details

Journal
Microbiology Spectrum
Published
2024-10-22
DOI
https://doi.org/10.1128/spectrum.01351-24
Citations
4
Primary Topic
Herpesvirus Infections and Treatments
Type
article
Field-Weighted Citation Impact
1.55

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article

The host cells suppress the proliferation of pseudorabies virus by regulating the PI3K/Akt/mTOR pathway

Yuancheng Zhou, Qian Tao, Zhiwen Xu, Feng-qin Lee et al.
4 citations
Microbiology Spectrum
Herpesvirus Infections and Treatments
1.55
article

The host cells suppress the proliferation of pseudorabies virus by regulating the PI3K/Akt/mTOR pathway

Yuancheng Zhou, Qian Tao, Zhiwen Xu, Feng-qin Lee, Zhijie Jian, Ling Zhu, Siyuan Lai, Lei Xu, Jun Zhao, Tong Xu, Li-shuang Deng, Yang Zhang
article en
4 citations

Abstract

PRV, known for its neurotropic properties, is capable of inducing severe neuronal damage. Our study discovered that following PRV infection, the expression of MMP2 was upregulated, leading to the degradation of ZO-1. Furthermore, upon PRV infection in the host, the promoter of TIMP1 is significantly activated, resulting in a significant increase in TIMP1 protein levels. This upregulation of TIMP1 inhibits the proliferation of PRV through the PI3K/Akt signaling pathway. This study elucidated the mechanism through which PRV, including the PRV XJ delgE/gI/TK strains, compromises the blood-brain barrier and identifies the antiviral response characterized by the activation of the PI3K/Akt signaling pathway within infected host cells. These findings provide potential therapeutic targets for the clinical management and treatment of PRV.

Microbiology SpectrumVol. 12(12)
Sichuan Agricultural University (CN), Sichuan Animal Science Academy (CN)
Sichuan Province Science and Technology Support Program, Sichuan Veterinary Medicine and Drug Innovation Group of China Agricultural Research System
Good health and well-being
Openalex Percentile: Top 16%
Herpesvirus Infections and Treatments
1.55
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The host cells suppress the proliferation of pseudorabies virus by regulating the PI3K/Akt/mTOR pathway — Yuancheng Zhou, Qian Tao, et al. · Microbiology Spectrum (2024) | TGRS Research Map | TGRS