ArticleFrontiers in microbiology2017
Japanese Encephalitis Virus Exploits Dopamine D2 Receptor-phospholipase C to Target Dopaminergic Human Neuronal Cells.
Article in Frontiers in microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Systemic review of CNS involvement and its manifestations in SARS-CoV2 positive patients.Journal of infection and public health · 2021Pooled it
- Crosstalk between vimentin and keratins in viral infection: Implications across the viral life cycle.Virulence · 2026Review
- Article
- 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
- Japanese encephalitis virus activates the NLRP3/caspase-1/GSDMD signaling pathway in dopaminergic neurons.PLoS neglected tropical diseases · 2026Article
- Vimentin Dynamics in Viral Infection: Shield or Sabotage?International journal of molecular sciences · 2025Review
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- Viruses and psychiatric disorders: We have not crossed the borderline from hypothesis to proof yet (Review).Molecular medicine reports · 2025Review
- Dopaminergic Perturbation in the Aetiology of Neurodevelopmental Disorders.Molecular neurobiology · 2025Review
- Repurposing Neurological Drugs Against Dengue Virus Infection.Journal of tropical medicine · 2025Review
- Alpha-synuclein expression in neurons modulates Japanese encephalitis virus infection.Journal of virology · 2024Article
- Quantification of the interaction forces between dengue virus and dopamine type-2 receptor using optical tweezers.Virology journal · 2024Article
- Screening a neurotransmitter-receptor-related inhibitor library identifies clomipramine HCl as a potential antiviral compound against Japanese encephalitis virus.Infectious medicine · 2024Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Characterization of the brain virome in human immunodeficiency virus infection and substance use disorder.PloS one · 2024Article
- Vector-Transmitted Flaviviruses: An Antiviral Molecules Overview.Microorganisms · 2023Review
- Coronavirus Porcine Epidemic Diarrhea Virus Utilizes Chemokine Interleukin-8 to Facilitate Viral Replication by Regulating CaJournal of virology · 2023Article
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Molecular Mechanism and Role of Japanese Encephalitis Virus Infection in Central Nervous System-Mediated Diseases.Viruses · 2022Review
- Improved survival in intensive care unit in severe COVID-19 associated with amantadine use - retrospective study.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the availability of vaccines for Japanese encephalitis virus (JEV), the re-emerging virus remains a clinically important pathogen that causes acute encephalitis and permanent neuropsychiatric sequels. JEV highly targets dopaminergic neuron-rich brain regions including the thalamus and midbrain. The molecular mechanism contributing to the high susceptibility of these particular brain regions remains largely unclear. This study addressed whether this tissue tropism of JEV is associated with signaling of dopaminergic neurons. Three pieces of evidence indicate that JEV exploits dopamine signaling to facilitate its infection: (1) JEV infection modulates dopamine level; (2) a selective dopamine D2 receptor (D2R) agonist enhances JEV infection; and (3) stimulation of D2R activates phospholipase C (PLC) to enhance the surface expression of JEV binding/entry molecules, integrin β3 and vimentin. Overall, JEV may exploit dopamine-mediated neuronal communication to increase the susceptibility of D2R-expressing cells to JEV infection. This study identifies a potential underlying mechanism of viral invasiveness in the dopaminergic brain regions and suggests antiviral strategies against viral infection by targeting D2R-PLC signaling.
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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.