Dengue virus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR067440_1.fastq.gz | Fastqsanger.gz | |||
| DRR067440_2.fastq.gz | Fastqsanger.gz | |||
| DRR067441_1.fastq.gz | Fastqsanger.gz | |||
| DRR067441_2.fastq.gz | Fastqsanger.gz | |||
| DRR067442_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Comprehensive study on virus quasi-species and vascular permeability factors in severe dengue infection in humans for innovative epidemic and clinical managements
| PRJDB5114 | ENA
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 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:Typical symptoms of uncomplicated dengue fever (DF) include headache, muscle pains, rash, cough, and vomiting. A proportion of cases progress to severe dengue hemorrhagic fever (DHF), associated with vascular permeability, thrombocytopenia, and hemorrhages. Progression to severe dengue is difficult to diagnose at the onset of fever, which complicates patient triage, posing a socio-economic burden on health systems. To identify parameters associated with protection and susceptibility to DHF, we pursued a systems immunology approach integrating plasma chemokine profiling, high-dimensional mass cytometry and peripheral blood mononuclear cell transcriptomic analysis at the onset of fever in a prospective study conducted in Indonesia.
2023-04-13 | GSE215835 | GEO
Project description:Plasmablats are the key cell type involved in Antibody (Ab) production that massively expand in dengue. However, little is known about their molecular profile in dengue . We investigated the transcriptional profiles of plasmablasts from dengue patients. We found that in addition to Ab secretion, they overexpress several molecules related to endothelial interactions, homing to skin or mucosal tisues. Additionally, there are hints for potential involvement in processes such as angiogenesis, leukocyte extravasation and vascular permeability. This is the fisrt detailed transcriptional analysis of plasmablast from dengue patients in India. We use flow cytometry to phenotype these cells and bulk RNA sequencing to analyze their transcriptinal profiles.
2021-09-13 | GSE171487 | GEO
Project description:Dengue virus infection can result in severe symptoms including shock and hemorrhage, but an understanding of the molecular correlates of disease severity is lacking. Bulk transcriptomics on blood samples are difficult to interpret because the blood is composed of different cell types that may react differently to virus infection. Dengue virus RNA can be detected in human plasma, however identifying the cells carrying dengue virus through the bloodstream in vivo has proven challenging. Here we used our recently developed viscRNA-Seq approach to profile transcriptomes of thousands of single blood peripheral mononuclear cells from 6 human subjects with dengue fever and severe dengue, as well as to characterize the cell types associated with dengue virus in the human blood. We found that although no bulk transcriptome marker for severe dengue exists, the expression of MX2 in naive B cells, of CD163 in CD14+/CD16+ monocytes and of other genes in specific cell types is highly predictive for severe dengue. We detected virus-associated cells in the blood of two severe dengue patients with high viral load and discovered the majority of these to be B cells expressing germline IgM or IgD immunoglobulin chains and naive markers but also showing signs of activation and expression of CD69, CXCR4, and other surface receptors. In bystander B cells we detected signs of strong immune activation, parallel hypersomatic evolution and, in one severe degue subject, an anomalously large clone of highly mutated, IgG1 plasmablasts that could be reactive to dengue virus. This study presents a high-resolution molecular exploration into dengue virus infection in humans and can be generalized to any RNA virus.
2018-11-19 | GSE116672 | GEO
Project description:Our hypothesis is that dengue induces different innate immune responses in patients with mild respective severe dengue. We further hypothesize that severe dengue infection is a consequence of an over reactive inflammatory response which could be inhibited in an early stage by immune suppressants. We hypothesize that the drugs used in this study induce a down regulated inflammatory response; VP-16 by triggering apoptosis and Rosiglitazone by inhibiting NFkB related cytokine production In-vitro dengue infected U937, transcriptional assessment
2014-04-01 | E-GEOD-28985 | biostudies-arrayexpress
Project description:Background: dengue is a potentially life-threatening viral infection. Early prognostic markers of severe complications may improve case management and reduce dengue-related mortalities. This study aimed to identify circulating microRNAs (miRNAs) as biomarkers for predicting severe dengue. Methods: Serum samples from dengue-infected patients were collected on the first day of admission. Patients were followed up for 14 days after admission to determine the final diagnosis. Participants were divided into non-severe and severe dengue, as defined by WHO 2009 criteria. Circulating microtranscriptome analysis was performed using the NanoString miRNA Expression Assay. The expression level of candidate miRNAs were then validated by quantitative reverse transcription-PCR (qRT-PCR) method. Findings: The discovery cohort (N=19) lead to the identification of 37 differentially expressed miRNAs between the two groups. Six miRNAs (miR122-5p, miR1246, miR1303, miR574-5p, miR30d-5p, and miR424-5p) were selected and further validated in the larger cohort (N=135). The qRT-PCR analysis confirmed that the six miRNAs expression levels were significantly higher in the severe dengue group compared to the non-severe group. Based on receiver operating characteristic (ROC) analysis, miR574-5p and miR1246 displayed the highest diagnostic performance in discriminating between severe from non-severe dengue (AROC curve =0·83). Additionally, miR574-5p and miR1246 had high sensitivity and high negative predictive value for detecting severe dengue. Multivariate analysis suggested that serum miR574-5p was an independent predictor of severe dengue (odds ratio 3·30, 95% CI 1·81-6·04; p<0·001). Interpretation: Circulating miRNAs, especially miR-574-5p and miR-1246, could be promising diagnostic and prognostic biomarkers for severe dengue.
2022-10-26 | GSE190749 | GEO
Project description:Our hypothesis is that dengue induces different innate immune responses in patients with mild respective severe dengue. We further hypothesize that severe dengue infection is a consequence of an over reactive inflammatory response which could be inhibited in an early stage by immune suppressants. We hypothesize that the drugs used in this study induce a down regulated inflammatory response; VP-16 by triggering apoptosis and Rosiglitazone by inhibiting NFkB related cytokine production
2014-04-01 | GSE28985 | GEO
Project description:Background: Dengue virus (DENV) infection induces various clinical manifestations and even causes organ injuries, leading to severe dengue haemorrhagic fever and dengue shock syndrome. Hepatic dysfunction was identified as a risk predictor of progression to severe disease during the febrile phase of dengue. However, the underlying mechanisms of hepatic injury remain unclear. Methods: A model of dengue disease was established in IFNAR−/− C57BL/6 mice by challenge with DENV-2. Body weight, symptoms, haematological parameters and liver pathological observations in mice were used to determine the effects of DENV infection. Liver transcriptome sequencing was performed to evaluate the features of the host response FNAR mice challenged with DENV. Functional enrichment analysis and analysis of significantly differentially expressed genes (DEGs) were used to determine the critical molecular mechanism of hepatic injury. Results: We observed haemoconcentration, leukopenia and liver pathologies in mice, consistent with findings in clinical dengue patients. Some differences in gene expression and biological processes were identified in this study. Transcriptional patterns in the liver indicated that antiviral responses to DENV and tissue damage via abnormal expression of proinflammatory cytokines were induced. Further analysis showed that the upregulated DEGs were significantly enriched in the leukocyte transendothelial migration, complement and coagulation cascades, and cytokine-cytokine receptor interactions signalling pathways, which are considered to be closely associated with the pathogenic mechanism of dengue. IL6, IL 10, ICAM-1, VCAM-1, MMP9 and NLRP3 were identified as biomarkers of progression to severe disease. Conclusions: The interactions of these cytokines, which activate inflammatory signalling, may lead to organ injury and haemoconcentration and even to vascular leakage in tissues, including the mouse liver. Our study identifies candidate host targets that could be used for further functional verification. In this study, we aimed to evaluate the transcriptomics features of liver injury in a mouse model of dengue virus infection based on a lethal animal model, and then perform a series of functional analyses to partially elucidate the underlying pathogenesis of DENV-induced liver injury.
2022-08-18 | GSE210022 | GEO