ArticleJournal of virology2013
Chandipura virus induces neuronal death through Fas-mediated extrinsic apoptotic pathway.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Chandipura Virus: An Emerging Neurological Threat Transmitted by Sandflies in India.Immunity, inflammation and disease · 2026Review
- Genomic and evolutionary characterization of Chandipura virus: a cause of the 2024 outbreak in Gujarat, India.Microbiology spectrum · 2026Article
- Emergence of Chandipura viral encephalitis in India: a strategic approach to combat a fatal viral epidemic.Annals of medicine and surgery (2012) · 2026Review
- A dominant role of cell death in limiting Chandipura virus propagation at cell-saturating high multiplicity of infection.bioRxiv : the preprint server for biology · 2025Article
- Characterisation of the virome ofThe Journal of general virology · 2025Article
- Re-emergingVirusdisease · 2024Review
- Fas/FasL-Mediated Apoptosis and Inflammation Contribute to Recovery from HSV-2-Mediated Spinal Cord Infection.Viruses · 2024Article
- Chandipura viral glycoprotein (CNV-G) promotes Gectosome generation and enables delivery of intracellular therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Diversity of sandflies in Vidarbha region of Maharashtra, India, a region endemic to Chandipura virus encephalitis.The Indian journal of medical research · 2023Article
- Apoptosis and Phagocytosis as Antiviral Mechanisms.Sub-cellular biochemistry · 2023Article
- Article
- Chandipura virus induces cell death in cancer cell lines of human origin and promotes tumor regressionMolecular therapy oncolytics · 2021Article
- Chandipura virus dysregulates the expression of hsa-miR-21-5p to activate NF-κB in human microglial cells.Journal of biomedical science · 2021Article
- Fas/FasL Contributes to HSV-1 Brain Infection and Neuroinflammation.Frontiers in immunology · 2021Article
- Chandipura Virus Utilizes the Prosurvival Function of RelA NF-κB for Its Propagation.Journal of virology · 2019Article
- Temperature sensitivity and environmental stability of Chandipura virus.Virusdisease · 2019Article
- Chandipura Viral Encephalitis: A Brief Review.The open virology journal · 2018Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chandipura virus (CHPV; genus Vesiculovirus, family Rhabdoviridae) is an emerging tropical pathogen with a case fatality rate of 55 to 75% that predominantly affects children in the age group of 2 to 16 years. Although it has been established as a neurotropic virus causing encephalitis, the molecular pathology leading to neuronal death is unknown. The present study elucidates for the first time the mechanism of cell death in neurons after CHPV infection that answers the basic cause of CHPV-mediated neurodegeneration. Through various cell death assays in vitro and in vivo, a relationship between viral replication within neuron and neuronal apoptosis has been established. We report that expression of CHPV phosphoprotein increases up to 6 h postinfection and diminishes thereafter in neuronal cell lines, signifying the replicative phase of CHPV. Various analyses conducted during the investigation established that CHPV-infected neurons are undergoing apoptosis through an extrinsic pathway mediated through the Fas-associated death domain (FADD) following activation of caspase-8 and -3 and prominent cleavage of poly(ADP-ribose) polymerase (PARP). Knocking down the expression of caspase-3, the final executioner of apoptosis, in a neuronal cell line by endoribonuclease-prepared small interfering RNA (siRNA) validated its pivotal role in CHPV-mediated neurodegeneration by showing reduction in apoptosis after CHPV infection.
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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.