ArticleJournal of neurovirology2010
Caspase-3 activation is required for reovirus-induced encephalitis in vivo.
Article in Journal of neurovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 40 citations in OpenAlex.
- The role of immune regulation in peripheral nerve regeneration: functions of inflammatory cells and cytokines.Frontiers in pharmacology · 2026Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Cell Killing by Reovirus: Mechanisms and Consequences.Current topics in microbiology and immunology · 2023Review
- Viral-mediated activation and inhibition of programmed cell death.PLoS pathogens · 2022Review
- Reovirus Activated Cell Death Pathways.Cells · 2022Review
- Upregulation of Glutaminyl Cyclase Contributes to ERS-Induced Apoptosis in PC12 Cells.BioMed research international · 2022Article
- Article
- The synergistic anticancer effects of ReoT3D, CPT-11, and BBI608 on murine colorectal cancer cells.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Article
- Noncanonical Cell Death Induction by Reassortant Reovirus.Journal of virology · 2020Article
- Article
- Impact of caspase-1/11, -3, -7, or IL-1Cell death discovery · 2017Article
- Mitochondrial p53 Contributes to Reovirus-Induced Neuronal Apoptosis and Central Nervous System Injury in a Mouse Model of Viral Encephalitis.Journal of virology · 2016Article
- Alpha-Synuclein Expression Restricts RNA Viral Infections in the Brain.Journal of virology · 2015Article
- Viral gene expression potentiates reovirus-induced necrosis.Virology · 2015Article
- Oncolytic reovirus preferentially induces apoptosis in KRAS mutant colorectal cancer cells, and synergizes with irinotecan.Oncotarget · 2014Article
- Article
- Bacterial infection increases periodontal bone loss in diabetic rats through enhanced apoptosis.The American journal of pathology · 2013Article
- Article
- Daxx upregulation within the cytoplasm of reovirus-infected cells is mediated by interferon and contributes to apoptosis.Journal of virology · 2013Article
- Survivin prevents apoptosis by binding to caspase-3 in astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus.Journal of neurovirology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Reovirus infection of neonatal mice provides a classic experimental system for understanding the molecular pathogenesis of central nervous system (CNS) viral infection. CNS tissue injury, caused by many human neurotropic viruses, including herpes viruses and West Nile virus, is associated with caspase-dependent apoptotic neuronal cell death. We have previously shown that reovirus-induced CNS tissue injury results from apoptosis and is associated with activation of both death-receptor and mitochondrial apoptotic pathways culminating in the activation of the downstream effector caspase, caspase-3. In order to directly investigate the role of caspase-3 in virus-induced neuronal death and CNS tissue injury during encephalitis, we have compared the pathogenesis of reovirus CNS infection in mice lacking the caspase-3 gene (caspase-3 (-/-)) to syngeneic wild-type mice. Prior studies of antiapoptotic treatments for reovirus-infected mice have indicated that protection from reovirus-induced neuronal injury can occur without altering the viral titer in the brains of infected mice. We now show that reovirus infection of caspase-3 (-/-) mice was associated with dramatic reduction in severity of CNS tissue injury, decreased viral antigen and titer in the brain, and enhanced survival of infected mice. Following intracerebral inoculation, the authors also show that virus spread from the brain to the eyes in reovirus-infected caspase-3 (-/-) mice, indicating that viral spread was intact in these mice. Examination of brains of long-term survivors of reovirus infection among caspase-3 (-/-) mice showed that these mice eventually clear their CNS viral infection, and do not manifest residual or delayed CNS tissue 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.