ArticleJournal of virology1999
Activation of caspases and p53 by bovine herpesvirus 1 infection results in programmed cell death and efficient virus release.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 123 citations in OpenAlex.
- Bovine α-herpesvirus 1 replication and immediate early transcription unit 1 promoter are jointly stimulated by glucocorticoid receptor and DNA-dependent ATPases.The Journal of general virology · 2026Article
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 2026Review
- Glycyrrhizin alleviates varicellovirus bovinealpha 1-induced oxidative stress, inflammation, and apoptosis in MDBK cells by inhibiting NF-κB/NLRP3 axis through the Nrf2 signalling pathway.Veterinary research communications · 2024Article
- Specificity protein 1 (Sp1) and glucocorticoid receptor (GR) stimulate bovine alphaherpesvirus 1 (BoHV-1) replication and cooperatively transactivate the immediate early transcription unit 1 promoter.Journal of virology · 2024Article
- Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death.Frontiers in immunology · 2022Article
- Apoptosis in the late replication phase of Bovine alphaherpesvirus 1 in experimentally infected calves.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021Article
- Article
- Inhibitory effect of silver nanoparticles on bovine herpesvirus-1.International journal of veterinary science and medicine · 2018Article
- The Major Tegument Protein of Bovine Herpesvirus 1, VP8, Interacts with DNA Damage Response Proteins and Induces Apoptosis.Journal of virology · 2018Article
- Programmed cell death: the battlefield between the host and alpha-herpesviruses and a potential avenue for cancer treatment.Oncotarget · 2018Review
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin influences bovine herpesvirus 1 replication through upregulation of SIRT3 and cytoskeletal reorganization.Veterinary research communications · 2017Article
- MG-132 reduces virus release in Bovine herpesvirus-1 infection.Scientific reports · 2017Article
- BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells.Veterinary research · 2016Article
- The ectopic expression of Snail in MDBK cells does not induce epithelial-mesenchymal transition.International journal of molecular medicine · 2015Article
- The effect of bovine viral diarrhea virus (BVDV) strains on bovine monocyte-derived dendritic cells (Mo-DC) phenotype and capacity to produce BVDV.Virology journal · 2014Article
- Bovine Herpes Virus 1 (BHV-1) and Herpes Simplex Virus Type 1 (HSV-1) Promote Survival of Latently Infected Sensory Neurons, in Part by Inhibiting Apoptosis.Journal of cell death · 2013Review
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin promotes BHV-1 infection in mammalian cells by interfering with iron homeostasis regulation.PloS one · 2013Article
- Bovine herpes virus type 1 induces apoptosis through Fas-dependent and mitochondria-controlled manner in Madin-Darby bovine kidney cells.Virology journal · 2012Article
- p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.PloS one · 2012Article
- Regulation of the latency-reactivation cycle by products encoded by the bovine herpesvirus 1 (BHV-1) latency-related gene.Journal of neurovirology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death (PCD), or apoptosis, is initiated in response to various stimuli, including virus infection. Bovine herpesvirus 1 (BHV-1) induces PCD in peripheral blood mononuclear cells at the G0/G1 phase of the cell cycle (E. Hanon, S. Hoornaert, F. Dequiedt, A. Vanderplasschen, J. Lyaku, L. Willems, and P.-P. Pastoret, Virology 232:351-358, 1997). However, penetration of virus particles is not required for PCD (E. Hanon, G. Meyer, A. Vanderplasschen, C. Dessy-Doize, E. Thiry, and P. P. Pastoret, J. Virol. 72:7638-7641, 1998). The mechanism by which BHV-1 induces PCD in peripheral blood mononuclear cells is not understood, nor is it clear whether nonlymphoid cells undergo PCD following infection. This study demonstrates that infection of bovine kidney (MDBK) cells with BHV-1 leads to PCD, as judged by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling, DNA laddering, and chromatin condensation. p53 appears to be important in this process, because p53 levels and promoter activity increased after infection. Expression of proteins that are stimulated by p53 (p21(Waf1) and Bax) is also activated after infection. Cleavage of Bcl-xL, a protein that inhibits PCD, occurred after infection, suggesting that caspases (interleukin-1beta-converting enzyme-like proteases) were activated. Other caspase substrates [poly(ADP-ribose) polymerase and actin] are also cleaved during the late stages of infection. Inhibition of caspase activity delayed cytotoxic activity and virus release but increased the overall virus yield. Taken together, these results indicate that nonlymphoid cells undergo PCD near the end of productive infection and further suggest that caspases enhance virus release.
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