ArticleFrontiers in cellular and infection microbiology2025
Japanese encephalitis virus-associated human microglia induce cell death of human microvascular endothelial cells in receptor-independent infection.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Marine-Derived Natural Products Against Flaviviruses: Mechanisms, Evidence, and Future Directions.Marine drugs · 2026Review
- Neuroinflammation and blood-brain barrier disruption in Japanese encephalitis virus infection: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2026Review
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6 authors.
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Abstract
Introduction: The neurotropic virus Japanese encephalitis virus invades the human central nervous system, inducing neuroinflammation and further disruption of the blood-brain barrier. JEV interacts with various cell types of the blood-brain barrier including the endothelial cells. The present work aims to investigate impact of receptor-dependent and independent infection of human microvascular endothelial cells by Japanese encephalitis virus. Methods: Receptor-dependent infection was achieved using cell-free virus while receptor-independent infection was by co-culture of microvascular endothelial cells with virus-associated microglia. Results: While both receptor-dependent and independent infections of human microvascular endothelial cells led to virus propagation, only receptor-independent infection induced cell death of human microvascular endothelial cells. While the CX Discussion: Overall, our findings demonstrate that human microvascular endothelial cells supply virus propagation and Japanese encephalitis virus-associated microglia greatly contribute to endothelial cell death, an important component of the blood brain barrier integrity. Importantly, Tumour Necrosis Factor-related apoptosis inducing ligand and receptors represents a promising therapeutic target preventing microvascular endothelial cell death after neuroinvasion.
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