2. Academic Validation
  3. PGK1 enhances productive bovine herpesvirus 1 infection by stimulating β-catenin-dependent transcription

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

  • Vet Res. 2025 Mar 7;56(1):50. doi: 10.1186/s13567-025-01480-5.
Xuan Li # 1,  Wenyuan Gu # 2,  Shitao Li 3,  Filomena Fiorito 4,  Xiuyan Ding 5,  Liqian Zhu 6
Affiliations

Affiliations

  • 1 Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei University, Baoding, 071002, China.
  • 2 Center for Animal Diseases Control and Prevention of Hebei Province, Shijiazhuang, 050035, China.
  • 3 Department of Microbiology and Immunology, Tulane University, New Orleans, LA, 70118, USA.
  • 4 Department of Veterinary Medicine and Animal Production, University of Naples Federico II, 80137, Naples, Italy.
  • 5 Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei University, Baoding, 071002, China. yding202201@163.com.
  • 6 Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei University, Baoding, 071002, China. lzhu3596@163.com.
  • # Contributed equally.
PMID: 40055833 DOI: 10.1186/s13567-025-01480-5
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.

Keywords

BoHV-1; PGK1; mitochondria; β-Catenin signalling.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-16665
    99.29%, Wnt Inhibitor
    Wnt
  • HY-15154
    99.88%, Cdc28p/Pho85p/PGK1 Inhibitor
    CDK