Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chronic Dengue Encephalitis in a Patient with Progressive Dementia

ABSTRACT: Dengue virus is the most common arbovirus worldwide and represents a significant public health concern. To date, chronic Dengue infections have not been previously reported. While investigating the etiology of central nervous system (CNS) disease in a patient presenting with progressive dementia, we elucidated a chronic dengue infection within the CNS. Comprehensive viral immune responses in both serum and cerebrospinal fluid (CSF) were profiled by a phage-display assay (VirScan). Enrichment of Dengue viral antibodies were detected in the CSF as compared to the serum. No virus was detected in serum or CSF, but post-mortem analysis confirmed Dengue virus in the brain by quantitative polymerase chain reaction (PCR), immunohistochemistry, RNAscope and sequencing. Dengue virus was detectable by PCR and sequencing from brain biopsy tissue collected 33 months ante-mortem, confirming a chronic infection. Comprehensive antibody profiling assays can aid in the diagnosis of encephalitis of unknown etiologies. Our findings suggest that Dengue virus infections may persist in the CNS and should be considered in patients with progressive dementia in endemic regions or with relevant travel history.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123125 | GEO | 2019/08/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chronic Dengue Encephalitis in a Patient with Progressive Dementia

Project description:Chronic Dengue Encephalitis in a Patient with Progressive Dementia

| PRJNA507605 | ENA

The effects of postmortem delay on mouse microglia gene expression

Project description:Microglia are specialized macrophages of the central nervous system (CNS) and first to react to pathogens or injury. Transcriptional profiling significantly contributed to our understanding of microglia functions. In the case of human CNS samples, a postmortem delay (PMD) in tissue access and collection is the potential factor that might affect microglia gene expression profiles. However, the direct analysis of effects of PMD on human microglia transcriptome is challenging due to many confounding factors such as sex, aging, nutrition, lifestyle, medication and medical history. To determine the effects of PMD on the microglia transcriptome. Here, we analyzed mouse microglia, where ante-mortem conditions and post-mortem delay can be tightly controlled. PMD had very limited effect on mouse microglia gene expression, only 50 genes (out of 15,554 detected genes) were differentially expressed between different PMDs.

2021-01-01 | GSE162209 | GEO

serum miRNAs among infants with dengue virus and influenza virus infection

Project description:serum miRNAs among infants with dengue virus and influenza virus infection

2015-03-31 | E-MTAB-3118 | biostudies-arrayexpress

Viral Detection Microarray Analysis of Unknown Tropical Febrile Illness Cases

Project description:This study aimed to use pan-viral detection microarrays to identify viruses in serum from cases of acute pediatric febrile illness in a tropical setting. Patient clinical data and serum samples were collected between 2005 and 2009 as part of an ongoing pediatric dengue virus study at the Hospital Infantil Manuel de Jesús Rivera in Managua, Nicaragua. This study focused on patients who presented with dengue-like illness but who tested negative for dengue-virus infection. We hypothesized that non-dengue viruses or previously uncharacterized viruses might be causing these illnesses. The Virochip microarray is capable of detecting known viruses and discovering novel viruses. This series includes 153 arrays corresponding to 148 cases and 5 HeLa controls. Keywords: viral detection, tropical febrile illness, dengue virus, Nicaragua, Virochip

2011-12-31 | GSE28142 | GEO

Viral Detection Microarray Analysis of Unknown Tropical Febrile Illness Cases

2011-12-31 | E-GEOD-28142 | biostudies-arrayexpress

Human primary macrophages infected with dengue virus serotype 2, strain 16681, and antibody-dependent enhancement of infection

Project description:Human primary monocytes were differentiated for 6days in the presence of M-CSF. The resulting macrophages were infected with dengue virus serotype 2, strain 16681 under the following conditions: Mock, Multiplicity of infection (MOI) 1 without antibodies, MOI 1 with 40ng/mL of irrelevant human antibody, MOI 1 with infection enhancing antibody (40ng/mL of a human monoclonal antibody against dengue), and either MOI 5 or MOI 2.5. Total cell RNA was isolated at 2h post infection or 24h post infection.

2014-12-30 | E-MTAB-3138 | biostudies-arrayexpress

Gene expression alterations in primary choroid plexus epithelial cells infected with JCPyV

Project description:The human polyomavirus, JCPyV, establishes a lifelong persistent infection in the peripheral organs of a majority of the human population worldwide. Patients who are immunocompromised due to underlying infections, cancer, or to immunomodulatory treatments for autoimmune disease are at risk for developing progressive multifocal leukoencephalopathy (PML) when the virus invades the CNS and infects macroglial cells in the brain parenchyma. It is not yet known how the virus enters the CNS to cause disease. The blood-choroid plexus barrier is a potential site of virus invasion as the cells that make up this barrier are known to be infected with virus both in vivo and in vitro. To understand the effects of virus infection on these cells we challenged primary choroid plexus epithelial cells with JCPyV and profiled changes in host gene expression. We found that JC infection induced the expression of proinflammatory chemokines and downregulated junctional proteins essential for maintaining blood-CSF and blood-brain barrier function. These data contribute to our understanding of how virus infection of the choroid plexus can modulate the host cell response to neuroinvasive pathogens.

2024-05-15 | GSE264236 | GEO

Induction of Pathogenic Sets of Genes in Macrophages and Neurons in NeuroAIDS

Project description:The etiology of the central nervous system (CNS) alterations after human immunodeficiency virus (HIV) infection, such as dementia and encephalitis, remains unknown. We have used microarray analysis in a monkey model of neuroAIDS to identify 98 genes, many previously unrecognized in lentiviral CNS pathogenesis, whose expression is significantly up-regulated in the frontal lobe of simian immunodeficiency virus-infected brains. Further, through immunohistochemical illumination, distinct classes of genes were found whose protein products localized to infiltrating macrophages, endothelial cells and resident glia, such as CD163, Glut5, and ISG15. In addition we found proteins induced in cortical neurons (ie, cyclin D3, tissue transglutaminase, 1-antichymotrypsin, and STAT1), which have not previously been described as participating in simian immunodeficiency virus or HIV-related CNS pathology. This molecular phenotyping in the infected brains revealed pathways promoting entry of macrophages into the brain and their subsequent detrimental effects on neurons. These data support the hypothesis that in HIV-induced CNS disease products of activated macrophages and astrocytes lead to CNS dysfunction by directly damaging neurons, as well as by induction of altered gene and protein expression profiles in neurons themselves which are deleterious to their function. Keywords = HIV dementia Keywords = Gene array Keywords = Simian immunodeficiency virus Keywords = rhesus macaque Keywords: other

2005-03-08 | GSE2377 | GEO

Identifying CNS-colonizing T cells as potential therapeutic targets to prevent progression of multiple sclerosis

Project description:Background: Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), can be suppressed in its early stages but eventually becomes clinically progressive and unresponsive to therapy. Here we investigate whether the therapeutic resistance of progressive MS can be attributed to chronic immune cell accumulation behind the blood brain barrier. Methods: We systematically track CNS-homing immune cells in the peripheral blood of 31 MS patients and 31 matched healthy individuals in an integrated analysis of 497,705 single cell transcriptomes and 355,433 surface protein profiles from 71 samples. Through spatial RNA-sequencing we localize these cells in post-mortem brain tissue of 6 progressive MS patients contrasted against 4 control brains (20 samples, 85,000 spot transcriptomes). Findings: We identify a specific pathogenic CD161+/LTB+ T cell population that resides in brains of progressive MS patients. Intriguingly, our data suggest that the colonization of the CNS by these T cells may begin earlier in the disease course, as they can be mobilized to the blood by usage of the integrin-blocking antibody natalizumab in relapsing-remitting MS patients. Conclusions: As a consequence, we lay the groundwork for a therapeutic strategy to deplete CNS-homing T cells before they can fuel treatment-resistant progression. Funding: This study was supported by funding from the University Medical Center Hamburg-Eppendorf, the Stifterverband für die Deutsche Wissenschaft, the OAK Foundation, Medical Research Council UK and Wellcome.

2021-02-16 | GSE144744 | GEO

Ribosome profiling analysis of Dengue Virus

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data