ArticleJournal of neuroinflammation2018
Activation of neuronal N-methyl-D-aspartate receptor plays a pivotal role in Japanese encephalitis virus-induced neuronal cell damage.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 84 citations in OpenAlex.
- Japanese encephalitis virus reprograms host pyrimidine metabolism to facilitate viral replication.Infectious medicine · 2026Article
- Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons.PLoS pathogens · 2026Article
- Neuroinflammation and blood-brain barrier disruption in Japanese encephalitis virus infection: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2026Review
- Anti-NMDA receptor encephalitis following Murray Valley encephalitis: a case report.ASM case reports · 2025Article
- NMDA receptor blockade attenuates Japanese encephalitis virus infection-induced microglia activation.Journal of neuroinflammation · 2024Article
- The glutamate receptor antagonist ifenprodil inhibits hepatitis E virus infection.Antimicrobial agents and chemotherapy · 2024Article
- Screening a neurotransmitter-receptor-related inhibitor library identifies clomipramine HCl as a potential antiviral compound against Japanese encephalitis virus.Infectious medicine · 2024Article
- Single-cell RNA sequencing reveals the immune features and viral tropism in the central nervous system of mice infected with Japanese encephalitis virus.Journal of neuroinflammation · 2024Article
- Article
- H3K27me3 of Rnf19a promotes neuroinflammatory response during Japanese encephalitis virus infection.Journal of neuroinflammation · 2023Article
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Roles of Fatty Acids in Microglial Polarization: Evidence from In Vitro and In Vivo Studies on Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Nucleotide-Binding Oligomerization Domain 1 (NOD1) Positively Regulates Neuroinflammation during Japanese Encephalitis Virus Infection.Microbiology spectrum · 2022Article
- Zika virus-induced TNF-α signaling dysregulates expression of neurologic genes associated with psychiatric disorders.Journal of neuroinflammation · 2022Article
- Kynurenine-3-monooxygenase (KMO) broadly inhibits viral infections via triggering NMDAR/Ca2+ influx and CaMKII/ IRF3-mediated IFN-β production.PLoS pathogens · 2022Article
- Calcium Ions Signaling: Targets for Attack and Utilization by Viruses.Frontiers in microbiology · 2022Review
- Pathogenicity and virulence of Japanese encephalitis virus: Neuroinflammation and neuronal cell damage.Virulence · 2021Review
- Enriched environment remedies cognitive dysfunctions and synaptic plasticity through NMDAR-CaAging · 2021Article
- Immunity to TBEV Related Flaviviruses with Reduced Pathogenicity Protects Mice from Disease but Not from TBEV Entry into the CNS.Vaccines · 2021Article
- The Causes and Long-Term Consequences of Viral Encephalitis.Frontiers in cellular neuroscience · 2021Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOverstimulation of glutamate receptors, especially neuronal N-methyl-D-aspartate receptor (NMDAR), mediates excitatory neurotoxicity in multiple neurodegenerative diseases. However, the role of NMDAR in the regulation of Japanese encephalitis virus (JEV)-mediated neuropathogenesis remains undisclosed. The primary objective of this study was to understand the function of NMDAR to JEV-induced neuronal cell damage and inflammation in the central nervous system.
methodsThe effect of JEV-induced NMDAR activation on the progression of Japanese encephalitis was evaluated using the primary mouse neuron/glia cultures and a mouse model of JEV infection. A high-affinity NMDAR antagonist MK-801 was employed to block the activity of NMDAR both in vitro and in vivo. The subsequent impact of NMDAR blockade was assessed by examining the neuronal cell death, glutamate and inflammatory cytokine production, and JEV-induced mice mortality.
resultsJEV infection enhanced the activity of NMDAR which eventually led to increased neuronal cell damage. The data obtained from our in vitro and in vivo assays demonstrated that NMDAR blockade significantly abrogated the neuronal cell death and inflammatory response triggered by JEV infection. Moreover, administration of NMDAR antagonist protected the mice from JEV-induced lethality.
conclusionNMDAR plays an imperative role in regulating the JEV-induced neuronal cell damage and neuroinflammation. Thus, NMDAR targeting may constitute a captivating approach to rein in Japanese encephalitis.
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