ArticleNeurochemical research2023
Japanese Encephalitis Virus Infection Causes an Imbalance in the Activation of Mitochondrial Fusion/Fission Genes and Triggers the Activation of NOX2-mediated Oxidative Stress and Neuronal Cell Death.
Article in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Virtual screening, molecular dynamics simulations, and antiviral evaluation of Ocimum basilicum phytoconstituents against Japanese encephalitis virus.Archives of virology · 2026Article
- ETV4 promotes ovarian cancer growth by regulating mitochondrial function through Mfn2 ubiquitination mediated by the E3 ubiquitin ligase MARCH9.Cell biology and toxicology · 2025Article
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- The Essential Role of Mitochondrial Dynamics in Viral Infections.International journal of molecular sciences · 2025Review
- Intracellular Iron Accumulation Induces Inflammatory and Oxidative Status of the Host After Japanese Encephalitis Viral Infection.Molecular neurobiology · 2024Article
- Flaviviruses manipulate mitochondrial processes to evade the innate immune response.Npj viruses · 2024Review
- Mitochondrial Dysfunction by FADDosome Promotes Gastric Mucosal Injury in Portal Hypertensive Gastropathy.International journal of biological sciences · 2024Article
- Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica.Parasites, hosts and diseases · 2023Article
- Virus-host Interactions in Early Japanese Encephalitis Virus Infection.Virus research · 2023Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria dysfunction may be an important contributor to Japanese encephalitis (JE) viral infection disease pathogenesis. In the current study, we define whether changes in mitochondrial DNA copy number (which is the biomarker for mitochondrial function) and alteration in mitochondria dynamics (fusion and fission) contribute to the pathology of the JE virus in vivo mice model. We found decreased mitochondria copy number, reduced activation of mitochondrial fission (FIS1/DRP1), and increased activation of mitochondrial fusion (MFN1/MFN2/OPA1) genes that are associated with increased NOX2-mediated ROS generation and neuronal cell death following JE virus infection. Furthermore, we found that antioxidant glutathione level decreases. In summary, the following study demonstrates that JE viral infection causes an imbalance in mitochondrial fission/fusion gene activation and promotes NOX2-mediated oxidative stress and cell death, suggesting that intervention in mitochondrial dynamics might be a potential therapeutic strategy for combating oxidative stress and inflammatory process in JE viral infection.
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Registered trials
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