ArticleJournal of virology2007
Caspase 3-dependent cell death of neurons contributes to the pathogenesis of West Nile virus encephalitis.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 180 citations in OpenAlex.
- Cellular Responses to Flavivirus Infections: Stress Signaling at the Crossroads of Host Defense and Virus Infection.Viruses · 2026Review
- Neuropathogenesis of Usutu virus-associated disease in Eurasian blackbirds (Turdus merula) involves apoptosis through the extrinsic pathway.Journal of neurovirology · 2026Article
- Role of innate immune and inflammatory signaling in West Nile virus tropism and neuronal and glial cell death.Scientific reports · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Sequelae of viral CNS infections including outcomes, mechanisms, and knowledge gaps.Npj viruses · 2025Review
- Emerging Arthropod-Borne Viruses Hijack the Host Cell Cytoskeleton During Neuroinvasion.Viruses · 2025Review
- Modes of action of a small molecule antiviral compound targeting yellow fever virus NS4B protein.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- West Nile Virus (WNV): One-Health and Eco-Health Global Risks.Veterinary sciences · 2025Review
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- An RBM10 and NF-κB interacting host lncRNA promotes JEV replication and neuronal cell death.Journal of virology · 2023Article
- ER stress induces caspase-2-tBID-GSDME-dependent cell death in neurons lytically infected with herpes simplex virus type 2.The EMBO journal · 2023Article
- Blockade of interferon signaling decreases gut barrier integrity and promotes severe West Nile virus disease.Nature communications · 2023Article
- Higher replication potential of West Nile virus governs apoptosis induction in human neuroblastoma cells.Apoptosis : an international journal on programmed cell death · 2023Article
- Pathological features of West Nile and Usutu virus natural infections in wild and domestic animals and in humans: A comparative review.One health (Amsterdam, Netherlands) · 2023Article
- Treatment with Granulocyte-Macrophage Colony-Stimulating Factor Reduces Viral Titers in the Brains of West Nile Virus-Infected Mice and Improves Survival.Journal of virology · 2023Article
- Review
- Exogenous Players in Mitochondria-Related CNS Disorders: Viral Pathogens and Unbalanced Microbiota in the Gut-Brain Axis.Biomolecules · 2023Review
- Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023Review
- Paradoxical roles for programmed cell death signaling during viral infection of the central nervous system.Current opinion in neurobiology · 2022Review
- Functional Analysis of the Cathepsin D Gene Response to SGIV Infection in the Orange-Spotted Grouper,Viruses · 2022Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
West Nile virus (WNV) is a neurotropic, arthropod-borne flavivirus that has become a significant global cause of viral encephalitis. To examine the mechanisms of WNV-induced neuronal death and the importance of apoptosis in pathogenesis, we evaluated the role of a key apoptotic regulator, caspase 3. WNV infection induced caspase 3 activation and apoptosis in the brains of wild-type mice. Notably, congenic caspase 3(-/-) mice were more resistant to lethal WNV infection, although there were no significant differences in the tissue viral burdens or the kinetics of viral spread. Instead, decreased neuronal death was observed in the cerebral cortices, brain stems, and cerebella of caspase 3(-/-) mice. Analogously, primary central nervous system (CNS)-derived neurons demonstrated caspase 3 activation and apoptosis after WNV infection, and treatment with caspase inhibitors or a genetic deficiency in caspase 3 significantly decreased virus-induced death. These studies establish that caspase 3-dependent apoptosis contributes to the pathogenesis of lethal WNV encephalitis and suggest possible novel therapeutic targets to restrict CNS injury.
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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.