ArticlePloS one2013
Infection of human endothelial cells by Japanese encephalitis virus: increased expression and release of soluble HLA-E.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Flavivirus Nonstructural Protein 1‑Driven Coagulation via Tissue Factor-Bearing Microvesicles: A Pilot Study.ACS omega · 2025Article
- Sequelae of viral CNS infections including outcomes, mechanisms, and knowledge gaps.Npj viruses · 2025Review
- Japanese encephalitis virus-associated human microglia induce cell death of human microvascular endothelial cells in receptor-independent infection.Frontiers in cellular and infection microbiology · 2025Article
- Natural killer (NK) cells in bipolar disorders.Neuroscience applied · 2024Review
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Alternative splicing and genetic variation of mhc-e: implications for rhesus cytomegalovirus-based vaccines.Communications biology · 2022Article
- Downregulated cytotoxic CD8Cellular & molecular immunology · 2022Article
- EGFR Activation Impairs Antiviral Activity of Interferon Signaling in Brain Microvascular Endothelial Cells During Japanese Encephalitis Virus Infection.Frontiers in microbiology · 2022Article
- HLA-E circulating and genetic determinants in schizophrenia and bipolar disorder.Scientific reports · 2021Article
- Ezrin is essential for the entry of Japanese encephalitis virus into the human brain microvascular endothelial cells.Emerging microbes & infections · 2020Article
- HLA Upregulation During Dengue Virus Infection Suppresses the Natural Killer Cell Response.Frontiers in cellular and infection microbiology · 2019Article
- Defining the role of NK cells during dengue virus infection.Immunology · 2018Review
- Upregulation of HLA-E by dengue and not Zika viruses.Clinical & translational immunology · 2018Article
- Regulation of inflammation in Japanese encephalitis.Journal of neuroinflammation · 2017Review
- Measuring antigen presentation in mouse brain endothelial cells ex vivo and in vitro.Nature protocols · 2015Article
- Autoimmune encephalitis and its relation to infection.Current neurology and neuroscience reports · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV) is a single stranded RNA virus that infects the central nervous system leading to acute encephalitis in children. Alterations in brain endothelial cells have been shown to precede the entry of this flavivirus into the brain, but infection of endothelial cells by JEV and their consequences are still unclear. Productive JEV infection was established in human endothelial cells leading to IFN-β and TNF-α production. The MHC genes for HLA-A, -B, -C and HLA-E antigens were upregulated in human brain microvascular endothelial cells, the endothelial-like cell line, ECV 304 and human foreskin fibroblasts upon JEV infection. We also report the release/shedding of soluble HLA-E (sHLA-E) from JEV infected human endothelial cells for the first time. This shedding of sHLA-E was blocked by an inhibitor of matrix metalloproteinases (MMP). In addition, MMP-9, a known mediator of HLA solubilisation was upregulated by JEV. In contrast, human fibroblasts showed only upregulation of cell-surface HLA-E. Addition of UV inactivated JEV-infected cell culture supernatants stimulated shedding of sHLA-E from uninfected ECV cells indicating a role for soluble factors/cytokines in the shedding process. Antibody mediated neutralization of TNF-α as well as IFNAR receptor together not only resulted in inhibition of sHLA-E shedding from uninfected cells, it also inhibited HLA-E and MMP-9 gene expression in JEV-infected cells. Shedding of sHLA-E was also observed with purified TNF-α and IFN-β as well as the dsRNA analog, poly (I:C). Both IFN-β and TNF-α further potentiated the shedding when added together. The role of soluble MHC antigens in JEV infection is hitherto unknown and therefore needs further investigation.
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