ArticleViruses2009
Regulation of Innate Immune Responses by Bovine Herpesvirus 1 and Infected Cell Protein 0 (bICP0).
Article in Viruses, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 56 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
- Recombinant Alphaherpesvirus Vectors in Veterinary Vaccinology: Platforms, Applications, and Translational Challenges.International journal of molecular sciences · 2026Review
- Bta-miR-146b promotes infectious bovine rhinotracheitis virus replication and inhibits type I interferon expression via targeting IRAK1.Frontiers in cellular and infection microbiology · 2026Article
- Glucocorticoid receptor occupancy of key bovine alphaherpesvirus 1 (BoHV-1) promoters correlates with chromatin remodeling during reactivation from latency.Journal of virology · 2025Article
- Human alpha-herpesvirus 1 (HSV-1) viral replication and reactivation from latency are expedited by the glucocorticoid receptor.Journal of virology · 2025Review
- Review
- A cell cycle regulator, E2F2, and glucocorticoid receptor cooperatively transactivate the bovine alphaherpesvirus 1 immediate early transcription unit 1 promoter.Journal of virology · 2024Article
- The Cell-Mediated Immune Response againstVaccines · 2023Review
- The Bovine Herpesvirus 1 Latency-Reactivation Cycle, a Chronic Problem in the Cattle Industry.Viruses · 2023Review
- DDIT3 antagonizes innate immune response to promote bovine alphaherpesvirus 1 replication via the DDIT3-SQSTM1-STING pathway.Virulence · 2022Article
- Progesterone Sporadically Induces Reactivation from Latency in Female Calves but Proficiently Stimulates Bovine Herpesvirus 1 Productive Infection.Journal of virology · 2022Article
- Comparative transcriptome analysis of MDBK cells reveals that BoIFN-γ augmented host immune responses to bovine herpesvirus 1 infection.Frontiers in microbiology · 2022Article
- Regulation of neurotropic herpesvirus productive infection and latency-reactivation cycle by glucocorticoid receptor and stress-induced transcription factors.Vitamins and hormones · 2021Article
- Progesterone increases the incidence of bovine herpesvirus 1 reactivation from latency and stimulates productive infection.Virus research · 2020Article
- The bovine herpesvirus 1 regulatory proteins, bICP4 and bICP22, are expressed during the escape from latency.Journal of neurovirology · 2019Article
- Bovine Herpesvirus 1 Counteracts Immune Responses and Immune-Surveillance to Enhance Pathogenesis and Virus Transmission.Frontiers in immunology · 2019Review
- The Involvement of Histone H3 Acetylation in Bovine Herpesvirus 1 Replication in MDBK Cells.Viruses · 2018Article
- Combinatorial Effects of the Glucocorticoid Receptor and Krüppel-Like Transcription Factor 15 on Bovine Herpesvirus 1 Transcription and Productive Infection.Journal of virology · 2017Article
- MG-132 reduces virus release in Bovine herpesvirus-1 infection.Scientific reports · 2017Article
- The role of phospholipase C signaling in bovine herpesvirus 1 infection.Veterinary research · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Bovine herpesvirus 1 (BoHV-1) infected cell protein 0 (bICP0) is an important transcriptional regulatory protein that stimulates productive infection. In transient transfection assays, bICP0 also inhibits interferon dependent transcription. bICP0 can induce degradation of interferon stimulatory factor 3 (IRF3), a cellular transcription factor that is crucial for activating beta interferon (IFN-β) promoter activity. Recent studies also concluded that interactions between bICP0 and IRF7 inhibit trans-activation of IFN-β promoter activity. The C3HC4 zinc RING (really important new gene) finger located near the amino terminus of bICP0 is important for all known functions of bICP0. A recombinant virus that contains a single amino acid change in a well conserved cysteine residue of the C3HC4 zinc RING finger of bICP0 grows poorly in cultured cells, and does not reactivate from latency in cattle confirming that the C3HC4 zinc RING finger is crucial for viral growth and pathogenesis. A bICP0 deletion mutant does not induce plaques in permissive cells, but induces autophagy in a cell type dependent manner. In summary, the ability of bICP0 to stimulate productive infection, and repress IFN dependent transcription plays a crucial role in the BoHV-1 infection cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.