ArticleCell death & disease2017
Japanese encephalitis virus induces human neural stem/progenitor cell death by elevating GRP78, PHB and hnRNPC through ER stress.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 81 citations in OpenAlex.
- RNF5 promotes acute lung injury through HSPA5 ER-to-cytosol translocation and resultant PERK activation.Cell death and differentiation · 2026Article
- Beyond the neuron: the role of glial cells in viral neuropathogenesis.Journal of virology · 2026Review
- Article
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Antiviral and neuroprotective activity of diallyl disulfide in Japanese encephalitis virus-challenged SH-SY5Y cells: a post-treatment approach for greater specificity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sequelae of viral CNS infections including outcomes, mechanisms, and knowledge gaps.Npj viruses · 2025Review
- The slow progression of Japanese encephalitis in aged mice is likely associated to B cell recruitment in the brain.Virologica Sinica · 2025Article
- Kinesin light chain 1 interacts with NS1 and is a susceptibility factor for dengue virus infection in mosquito cells.The Journal of general virology · 2025Article
- PARP-16 regulates the PERK and IRE-1α Mediated Unfolded Protein Response in Japanese Encephalitis Virus-Infected Neural Stem/Progenitor Cells.Molecular neurobiology · 2025Article
- Arboviruses: the hidden danger of the tropics.Archives of virology · 2025Review
- Viruses and psychiatric disorders: We have not crossed the borderline from hypothesis to proof yet (Review).Molecular medicine reports · 2025Review
- Prohibitins in infection: potential therapeutic targets.Future microbiology · 2025Review
- mAging and disease · 2024Article
- The interaction of GRP78 and Zika virus E and NS1 proteins occurs in a chaperone-client manner.Scientific reports · 2024Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Regulation of Onecut2 by miR-9-5p in Japanese encephalitis virus infected neural stem/progenitor cells.Microbiology spectrum · 2024Article
- Mechanisms of ferroptosis and the relationship between ferroptosis and ER stress after JEV and HSV infection.Frontiers in microbiology · 2024Review
- Sodium Butyrate Induced Neural Stem/Progenitor Cell Death in an Experimental Model of Japanese Encephalitis.Metabolic brain disease · 2023Article
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Machine learning reveals neutrophil-to-lymphocyte ratio as a crucial prognostic indicator in severe Japanese encephalitis patients.Frontiers in neurology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV), which is a causative agent of sporadic encephalitis, harbours itself inside the neural stem/progenitor cells. It is a well-known fact that JEV infects neural stem/progenitor cells and decreases their proliferation capacity. With mass spectrometry-based quantitative proteomic study, it is possible to reveal the impact of virus on the stem cells at protein level. Our aim was to perceive the stem cell proteomic response upon viral challenge. We performed a two-dimensional gel electrophoresis-based proteomic study of the human neural stem cells (hNS1 cell line) post JEV infection and found that 13 proteins were differentially expressed. The altered proteome profile of hNS1 cell line revealed sustained endoplasmic reticulum stress, which deteriorated normal cellular activities leading to cell apoptosis. The proteomic changes found in hNS1 cell line were validated in vivo in the subventricular zone of JE infected BALB/c mice. Congruent alterations were also witnessed in multipotent neural precursor cells isolated from human foetus and in autopsy samples of human brain clinically diagnosed as cases of JE patients. Endoplasmic reticulum resident chaperone GRP78, mitochondrial protein Prohibitin and heterogeneous nuclear ribonucleoprotein hnRNPC (C1/C2) have been shown to interact with viral RNA. Hence it is proposed that these are the principle candidates governing endoplasmic reticulum stress-induced apoptosis in JEV infection.
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