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.
- 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. [email protected].
- 6. Key Laboratory of Microbial Diversity Research and Application of Hebei Province, School of Life Sciences, Hebei University, Baoding, 071002, China. [email protected].
- # Contributed equally.
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.