ArticleJournal of neuroinflammation2023
H3K27me3 of Rnf19a promotes neuroinflammatory response during Japanese encephalitis virus infection.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Neuronal Apoptotic Bodies Facilitate Japanese Encephalitis Virus Infection and Pathogenicity.Journal of extracellular vesicles · 2026Article
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
- Neuroinflammation and blood-brain barrier disruption in Japanese encephalitis virus infection: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2026Review
- Ferroptosis contributes to JEV-induced neuronal damage and neuroinflammation.Virologica Sinica · 2024Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Histone methylation is an important epigenetic modification that affects various biological processes, including the inflammatory response. In this study, we found that infection with Japanese encephalitis virus (JEV) leads to an increase in H3K27me3 in BV2 microglial cell line, primary mouse microglia and mouse brain. Inhibition of H3K27me3 modification through EZH2 knockdown and treatment with EZH2 inhibitor significantly reduces the production of pro-inflammatory cytokines during JEV infection, which suggests that H3K27me3 modification plays a crucial role in the neuroinflammatory response caused by JEV infection. The chromatin immunoprecipitation-sequencing (ChIP-sequencing) assay revealed an increase in H3K27me3 modification of E3 ubiquitin ligases Rnf19a following JEV infection, which leads to downregulation of Rnf19a expression. Furthermore, the results showed that Rnf19a negatively regulates the neuroinflammatory response induced by JEV. This is achieved through the degradation of RIG-I by mediating its ubiquitination. In conclusion, our findings reveal a novel mechanism by which JEV triggers extensive neuroinflammation from an epigenetic perspective.
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Registered trials
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