MicroRNA expression analysis in Dengue virus infection
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PROVIDER: PRJNA715467 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression analysis in Dengue virus infection
| PRJNA720832 | ENA
Project description:Dengue virus is an + strand RNA virus. We have carried our infections of human cells with Dengue and analyzed the translation, replication, and localization of the Dengue RNA. This allowed for clear definition of the life cycle of the Dengue virus inside a host cell. We also assessed the host response to Dengue virus, finding that a large fraction of the translational response is due to Interferon function. Translational and transcriptional analysis of the cellular response to Dengue virus infection
2016-09-01 | E-GEOD-69602 | biostudies-arrayexpress
Project description:serum miRNAs among infants with dengue virus and influenza virus infection
2015-03-31 | E-MTAB-3118 | biostudies-arrayexpress
Project description:Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease. We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes. Early passage primary endothelial cells (HUVECs) were mock infected (no virus) or infected with dengue virus and total RNA collected at 3 timepoints: 12, 24, and 48 hours post infection. Multiple timepoints were analyzed to identify changes in gene expression levels over time. Gene expression from both mock infected and dengue virus infected endothelial cells was evaluated to determine fold induction at each timepoint.
2012-04-10 | E-GEOD-34628 | biostudies-arrayexpress
Project description:Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease. We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes.
2012-04-11 | GSE34628 | GEO
Project description:Dengue virus is an + strand RNA virus. We have carried our infections of human cells with Dengue and analyzed the translation, replication, and localization of the Dengue RNA. This allowed for clear definition of the life cycle of the Dengue virus inside a host cell. We also assessed the host response to Dengue virus, finding that a large fraction of the translational response is due to Interferon function.
2016-09-01 | GSE69602 | GEO
Project description:Whole blood from patients with acute dengue infection (as determined with PCR) were assessed for global transcriptional changes during different stages of the disease with reference to dengue virus IgG status at study inclusion
2014-04-01 | GSE28988 | GEO
Project description:Whole blood from patients with acute dengue infection (as determined with PCR) were assessed for global transcriptional changes during different stages of the disease with reference to dengue virus IgG status at study inclusion Whole blood collected in PAX-gene tubes and extracted for total RNA
2014-04-01 | E-GEOD-28988 | biostudies-arrayexpress
Project description:The goal of this study was to compare the transcriptional profile (RNA-seq) of Dengue virus 2 and mock infected cells at 24 and 36 hours post infection. Dengue virus NS5 protein plays multiple functions in the cytoplasm of infected cells, enabling viral RNA replication and counteracting host antiviral responses. Here, we demonstrate a novel function of NS5 in the nucleus where it interferes with cellular splicing. Using global proteomic analysis of infected cells together with functional studies, we found that NS5 binds spliceosome complexes and modulates endogenous splicing. In particular, we show that NS5 alone, or in the context of viral infection, interacts with core components of the U5 snRNP particle, CD2BP2 and DDX23, alters the inclusion/exclusion ratio of alternative splicing events, and changes mRNA isoform abundance of known antiviral factors. Interestingly, a genome wide transcriptome analysis, using recently developed bioinformatics tools, revealed an increase of intron retention upon dengue virus infection, and viral replication was improved by silencing specific U5 components. Different mechanistic studies indicate that binding of NS5 to the spliceosome reduces the efficiency of pre-mRNA processing, independently of NS5 enzymatic activities. We propose that NS5 binding to U5 snRNP proteins hijacks the splicing machinery resulting in a less restrictive environment for viral replication. A549 cells where infected with Dengue virus 2 or mock and after 24 and 36 hours post infection mRNA was purified. Then the transcriptional profile of these cells was analyzed using RNA-seq.
2016-08-09 | E-GEOD-84285 | biostudies-arrayexpress
Project description:Background: Organ dysfunction, especially liver injury, caused by dengue virus (DENV) infection has been associated with fatal cases in dengue patients around the world. However, the pathophysiological mechanisms of liver involvement in dengue remain unclear. There is accumulating evidence that miRNAs are playing an important role in regulating viral pathogenesis, and it can help in diagnostic and anti-viral therapies development. Methods: We collected liver tissues of DENV-infected for small RNA sequencing to identify significantly different express miRNAs during dengue virus infection, and the identified target genes of these miRNAs were annotated by biological function and pathway enrichment. Results: 31 significantly altered miRNAs were identified, including 16 up-regulated and 15 down-regulated miRNAs. By performing a series of miRNA prediction and signaling pathway enrichment analyses, the down-regulated miRNAs of mmu-miR-484, mmu-miR-1247-5p and mmu-miR-6538 were identified to be the crucial miRNAs. Further analysis revealed that the inflammation and immune responses involving Hippo, PI3K-Akt, MAPK, Wnt, mTOR, TGF-beta, Tight junction, and Platelet activation were modulated collectively by these three key miRNAs during DENV infection. These pathways are considered to be closely associated with the pathogenic mechanism and treatment strategy of dengue patients. Conclusion: The miRNAs identified by sequencing, especially miR-484 may be the potential therapeutic targets for liver involvement in dengue patients which involves the regulation of vascular permeability and expression of inflammatory cytokines. In this study, RNA-Seq analysis of liver tissues from a mouse model after DENV infection was performed to identify differential miRNA expression profiles, predicted target genes, and analyzed the biological functions and pathways involved in the regulation of differential miRNAs, contributing to the understanding of the mechanisms of liver tissue involvement after DENV infection.
2022-09-13 | GSE213107 | GEO