PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription

Abstract Bovine herpesvirus 1 (BoHV-1) productive infection stimulates β-catenin-dependent transcription to facilitate virus replication. Phosphoglycerate kinase 1 (PGK1), which catalyses the initial step of ATP production during glycolysis, also has a mitochondrial form that is implicated in tissue...

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Main Authors: Xuan Li, Wenyuan Gu, Shitao Li, Filomena Fiorito, Xiuyan Ding, Liqian Zhu
Format: Article
Language:English
Published: BMC 2025-03-01
Series:Veterinary Research
Subjects:
Online Access:https://doi.org/10.1186/s13567-025-01480-5
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author Xuan Li
Wenyuan Gu
Shitao Li
Filomena Fiorito
Xiuyan Ding
Liqian Zhu
author_facet Xuan Li
Wenyuan Gu
Shitao Li
Filomena Fiorito
Xiuyan Ding
Liqian Zhu
author_sort Xuan Li
collection DOAJ
description Abstract Bovine herpesvirus 1 (BoHV-1) productive infection stimulates β-catenin-dependent transcription to facilitate virus replication. Phosphoglycerate kinase 1 (PGK1), which catalyses the initial step of ATP production during glycolysis, also has a mitochondrial form that is implicated in tissue injury across various diseases. However, the relationship between BoHV-1 replication and the PGK1 signalling pathway is not yet fully understood. In this study, we discovered that PGK1 signalling significantly influences BoHV-1 replication, with the virus infection leading to a marked increase in the accumulation of PGK1 proteins in mitochondria. Overexpression of β-catenin reduces PGK1 steady-state protein levels while overexpressing PGK1 boosts β-catenin protein expression—a phenomenon that reverses upon virus infection. Importantly, consistent with PGK1’s vital role in virus replication, PGK1 stimulates β-catenin-dependent transcriptional activity, partly by promoting the nuclear accumulation of transcriptionally active β-catenin and phospho-β-catenin (S552) in virus-infected cells. In summary, our findings suggest for the first time that PGK1 signalling may be involved in BoHV-1 replication and contribute to virus pathogenicity.
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issn 1297-9716
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publishDate 2025-03-01
publisher BMC
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spelling doaj-art-38a8ce896e0e4e669099096f8a244f512025-08-20T01:57:27ZengBMCVeterinary Research1297-97162025-03-0156111610.1186/s13567-025-01480-5PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcriptionXuan Li0Wenyuan Gu1Shitao Li2Filomena Fiorito3Xiuyan Ding4Liqian Zhu5Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei UniversityCenter for Animal Diseases Control and Prevention of Hebei ProvinceDepartment of Microbiology and Immunology, Tulane UniversityDepartment of Veterinary Medicine and Animal Production, University of Naples Federico IIKey Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei UniversityKey Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei UniversityAbstract Bovine herpesvirus 1 (BoHV-1) productive infection stimulates β-catenin-dependent transcription to facilitate virus replication. Phosphoglycerate kinase 1 (PGK1), which catalyses the initial step of ATP production during glycolysis, also has a mitochondrial form that is implicated in tissue injury across various diseases. However, the relationship between BoHV-1 replication and the PGK1 signalling pathway is not yet fully understood. In this study, we discovered that PGK1 signalling significantly influences BoHV-1 replication, with the virus infection leading to a marked increase in the accumulation of PGK1 proteins in mitochondria. Overexpression of β-catenin reduces PGK1 steady-state protein levels while overexpressing PGK1 boosts β-catenin protein expression—a phenomenon that reverses upon virus infection. Importantly, consistent with PGK1’s vital role in virus replication, PGK1 stimulates β-catenin-dependent transcriptional activity, partly by promoting the nuclear accumulation of transcriptionally active β-catenin and phospho-β-catenin (S552) in virus-infected cells. In summary, our findings suggest for the first time that PGK1 signalling may be involved in BoHV-1 replication and contribute to virus pathogenicity.https://doi.org/10.1186/s13567-025-01480-5BoHV-1PGK1β-Catenin signallingmitochondria
spellingShingle Xuan Li
Wenyuan Gu
Shitao Li
Filomena Fiorito
Xiuyan Ding
Liqian Zhu
PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
Veterinary Research
BoHV-1
PGK1
β-Catenin signalling
mitochondria
title PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
title_full PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
title_fullStr PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
title_full_unstemmed PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
title_short PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription
title_sort pgk1 enhances productive bovine herpesvirus 1 infection by stimulating β catenin dependent transcription
topic BoHV-1
PGK1
β-Catenin signalling
mitochondria
url https://doi.org/10.1186/s13567-025-01480-5
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