ArticleVeterinary research2017
The role of phospholipase C signaling in bovine herpesvirus 1 infection.
Article in Veterinary research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- D-glucose uptake inhibits bovine alphaherpesvirus 1 post-binding cell process entry via inhibition of PLC-γ1 signaling in a glucose transporter 1-independent manner.Microbiology spectrum · 2026Article
- The immunosuppressive effects and mechanisms of loureirin B on collagen-induced arthritis in rats.Frontiers in immunology · 2023Article
- Differential expression profile and in-silico functional analysis of long noncoding RNA and mRNA in duck embryo fibroblasts infected with duck plague virus.BMC genomics · 2022Article
- Article
- Loureirin B Exerts its Immunosuppressive Effects by Inhibiting STIM1/Orai1 and KFrontiers in pharmacology · 2021Article
- Induction of the Unfolded Protein Response during Bovine Alphaherpesvirus 1 Infection.Viruses · 2020Article
- Dewormer drug fenbendazole has antiviral effects on BoHV-1 productive infection in cell cultures.Journal of veterinary science · 2020Article
- Article
- The Involvement of Histone H3 Acetylation in Bovine Herpesvirus 1 Replication in MDBK Cells.Viruses · 2018Article
- Analysis of microRNAs Expression Profiles in Madin-Darby Bovine Kidney Cells Infected With Caprine Parainfluenza Virus Type 3.Frontiers in cellular and infection microbiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine herpesvirus 1 (BoHV-1) infection enhanced the generation of inflammatory mediator reactive oxidative species (ROS) and stimulated MAPK signaling that are highly possibly related to virus induced inflammation. In this study, for the first time we show that BoHV-1 infection manipulated phospholipase C (PLC) signaling, as demonstrated by the activation of PLCγ-1 at both early stages [at 0.5 h post-infection (hpi)] and late stages (4-12 hpi) during the virus infection of MDBK cells. Viral entry, and de novo protein expression and/or DNA replication were potentially responsible for the activation of PLCγ-1 signaling. PLC signaling inhibitors of both U73122 and edelfosine significantly inhibited BoHV-1 replication in both bovine kidney cells (MDBK) and rabbit skin cells (RS-1) in a dose-dependent manner by affecting the virus entry stage(s). In addition, the activation of Erk1/2 and p38MAPK signaling, and the enhanced generation of ROS by BoHV-1 infection were obviously ameliorated by chemical inhibition of PLC signaling, implying the requirement of PLC signaling in ROS production and these MAPK pathway activation. These results suggest that the activation of PLC signaling is a potential pathogenic mechanism for BoHV-1 infection.
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