Transcriptome profiling of dendritic cells during JEV infection
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ABSTRACT:
PROVIDER: PRJNA672148 | ENA |
REPOSITORIES: ENA
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Project description:Characterization of transcriptional signature of innate immune response and metabolic pathways in monocytes derived dendritic cells (MoDCs) of healthy donors during JEV infection.
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Project description:Infection by neurotropic virus Japanese Encephalitis Virus (JEV) is characterized by profound neuronal cell death and neuroinflammation. Long non-coding RNAs (lncRNAs) are critical regulatory players in diverse biological processes, including viral pathogenesis. We use whole transcriptomic sequencing to identify a lncRNA JINR1 (JEV-induced non-coding RNA 1) induced upon JEV infection in neuronal cells. Transcription factor NF-κB triggers JINR-1 expression during JEV infection. Loss of JINR-1 impairs virus replication and reduces JEV-induced neuronal cell death and expression of genes involved in ER stress and neuroinflammation. Mechanistically, JINR1 inhibits the expression of mir-216-5p, which inhibits host factors GRP78 and c-JUN and the viral genome. In line with its role as a pro-viral host factor, JINR1 interacts with RBM10 and NF-κB to promote the expression of genes involved in ER stress and neuroinflammation. Our results suggest a role for JINR-1 in promoting JEV-induced cell death and neuroinflammation.
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Project description:B16F10, a murine melanoma cel line is cytolytic to JEV infection. We have identified a B16F10 cell line variant which is non-cytolytic to JEV infection. This variant cell line has two types of cells, one which is persistently infected JEV and another which is resistant to JEV infection. The JEV-resistant cells (B16F10r) were seperated from the presistently infected cells by single cell cloning. To understand the mechanism of JEV resistance microarray analysis was caried out to Identify and characterize genes differentially expressed during in uninfected/JEV-infected B16F10 and B16F10r cells. Agilent one-color experiment,Organism: Mus musculus ,Agilent Custom Mouse Whole Genome Mouse 8x60k Gene expression designed by Genotypic Technology Private Limited, Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
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Project description:Japanese encephalitis virus (JEV) is a causative agent of encephalitis, mostly prevalent in Asia and South-Asian countries. Neuroinflammation is the hallmark of encephalitis, mediated in parts through the activation of brain-resident microglial cell, thus playing a critical role in determining pathogenesis. Deregulated activity of microglia can be lethal for the brain tissue. Interferon Regulatory Factor 8 (Irf8) mediates differentiation and transformation of microglia to reactive phenotypes and also regulates antiviral response through cross-talk with interferon pathway. In this study, we have conducted a comparative study between JEV infected C57BL/6 wild type and Irf8 Knockout (IRF8-/-) to identify the genes directly or indirectly regulated by IRF8.
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Project description:Flaviviruses, particularly Japanese encephalitis virus (JEV) and West Nile virus (WNV), are important causes of virus-induced central nervous system (CNS) disease in humans. We used microarray analysis to identify cellular genes that are differentially regulated following infection of the brain with JEV (P3) or WNV (New York 99). Gene expression data for these flaviviruses was compared to that induced following infection of the brain with reovirus (Type 3 Dearing), an unrelated neurotropic virus. Although several studies have described gene expression changes following virus infection of the brain, this report is the first to directly compare large-scale gene expression data from different viruses. We found that a large number of genes were up-regulated in common to infections with all 3 viruses (fold change > 2, P < 0.001), including genes associated with interferon signaling, the immune system, inflammation and cell death/survival signaling. In addition, genes associated with glutamate signaling were down-regulated in common to infections with all 3 viruses (fold change > 2, P < 0.001). These genes may serve broad spectrum therapeutic targets for virus-induced CNS disease. A distinct set of genes were up-regulated following flavivirus-infection, but not following infection with reovirus. These genes were associated with tRNA charging and may serve as therapeutic targets for flavivirus-induce CNS disease.
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