ArticleJournal of virology2012
Critical role for voltage-dependent anion channel 2 in infectious bursal disease virus-induced apoptosis in host cells via interaction with VP5.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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
54 citing papers in PubMed, 92 citations in OpenAlex.
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- Infectious bursal disease virus induces GSDME-dependent pyroptosis via the mitochondrial caspase-9/3 pathway in DF-1 cells.Veterinary research · 2026Article
- Targeted molecular docking-guided insights into the antioxidant reparative mechanisms ofBiochemistry and biophysics reports · 2026Article
- Infectious bursal disease virus suppresses humoral immunity via blocking antibody affinity maturation in chickens.iScience · 2026Article
- Mapping Molecular Determinants of Antigenicity and Pathogenicity of Infectious Bursal Disease Virus (IBDV): A Scoping Review.Viruses · 2026Article
- Pathogenicity, immunogenicity, and multi-organ tissue tropism of a novel variant infectious bursal disease virus in specific pathogen-free chickens.Veterinary world · 2026Article
- Key role of TLR3 in type I IFN expression and apoptosis induction in IBDV-infected chicken fibroblast cells.Frontiers in cellular and infection microbiology · 2026Article
- Chicken caspase-3 promotes IBDV replication via the cleavage of IRF7.Frontiers in microbiology · 2026Article
- Chicken GSDME, a major pore-forming molecule responsible for RNA virus-induced pyroptosis in chicken.Journal of virology · 2025Article
- Decoding Cancer through Silencing the Mitochondrial Gatekeeper VDAC1.Biomolecules · 2024Review
- Reduced NR2F2 Expression in the Host Response to Infectious Bursal Disease Virus Infection Suppressed Viral Replication by Enhancing Type I Interferon Expression by Targeting SOCS5.Journal of virology · 2023Article
- Phosphorylation of VP1 Mediated by CDK1-Cyclin B1 Facilitates Infectious Bursal Disease Virus Replication.Journal of virology · 2023Article
- Advances on adaptive immune responses affected by infectious bursal disease virus in chicken.Frontiers in immunology · 2023Review
- Review
- Genetics and Pathogenicity of Natural Reassortant of Infectious Bursal Disease Virus Emerging in Latvia.Pathogens (Basel, Switzerland) · 2022Article
- Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses.Frontiers in immunology · 2022Review
- Protective effects of the NLRP3 inflammasome against infectious bursal disease virus replication in DF-1 cells.Archives of virology · 2021Article
- The Novel Genetic Background of Infectious Bursal Disease Virus Strains Emerging from the Action of Positive Selection.Viruses · 2021Article
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- Role of MicroRNAs in Host Defense against Infectious Bursal Disease Virus (IBDV) Infection: A Hidden Front Line.Viruses · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). Although IBDV-induced host cell apoptosis has been established, the underlying molecular mechanism is still unclear. We report here that IBDV viral protein 5 (VP5) is a major apoptosis inducer in DF-1 cells by interacting with the voltage-dependent anion channel 2 (VDAC2) in the mitochondrion. We found that in DF-1 cells, VP5-induced apoptosis can be completely abolished by 4,4'-diisothiocyanatostibene-2,2'-disulfonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by small interfering RNA markedly inhibits IBDV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome c release, leading to increased IBDV growth in host cells. Thus, VP5-induced apoptosis during IBDV infection is mediated by interacting with VDAC2, a protein that appears to restrict viral replication via induction of cell death.
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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.