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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
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Borna disease virus 1 induces ferroptosis, contributing to lethal encephalitis
Qing Tan1,2, Hongli Yang1,3, Yong He1,2
1NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Journal of Medical Virology
|October 7, 2024
Summary
Borna disease virus 1 (BoDV-1) infection triggers ferroptosis, a cell death pathway involving iron overload and lipid peroxidation. Inhibiting ferroptosis or the ubiquitin-proteasome system alleviates Borna disease virus 1 encephalitis (BVE) in models.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Borna disease virus 1 (BoDV-1) causes fatal encephalitis in humans.
- Ferroptosis, a form of programmed cell death, is implicated in viral infections.
- The role of ferroptosis in BoDV-1 encephalitis (BVE) pathogenesis is unclear.
Purpose of the Study:
- To investigate the link between BoDV-1 infection and ferroptosis.
- To elucidate the role of ferroptosis in BVE pathogenesis.
- To explore therapeutic strategies targeting ferroptosis in BVE.
Main Methods:
- Primary rat cortical neurons, human microglial cells, and Sprague-Dawley rats were used as models.
- Ferroptosis markers (iron overload, lipid peroxidation, ROS) were assessed.
- Gene and protein expression (qRT-PCR, Western blot) analyzed the Nrf2/HO-1/SLC7a11/GPX4 and PTGS2/PGE2 pathways.
- Inhibition of ferroptosis and the ubiquitin-proteasome system was tested.
Main Results:
- BoDV-1 infection induced ferroptosis characterized by iron overload, increased reactive oxygen species, and mitochondrial damage.
- BoDV-1 suppressed the Nrf2/HO-1/SLC7a11/GPX4 antioxidant pathway via Nrf2 ubiquitination and degradation.
- Activated PTGS2/PGE2 signaling and release of lipid peroxidation products contributed to BVE.
- Inhibiting ferroptosis or the ubiquitin-proteasome system reduced BVE severity.
Conclusions:
- BoDV-1 infection induces ferroptosis in neural cells.
- Suppression of the Nrf2/HO-1/SLC7a11/GPX4 pathway is a key mechanism in BoDV-1-induced ferroptosis.
- Ferroptosis is a critical pathogenic mechanism in BVE.
- Targeting ferroptosis and the ubiquitin-proteasome system offers potential therapeutic avenues for BVE.
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