Transcriptional Correlates of Tolerance and Lethality from Mouse Models Predict Ebola Virus Disease Outcome
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE130629 | GEO | 2019/12/01
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional Correlates of Tolerance and Lethality from Mouse Models Predict Ebola Virus Disease Outcome
| PRJNA540840 | ENA
Project description:<p align="left"><b>Title: </b> Ebola-infected non-human primates - PBMCs<br> <p align="left"><b>Summary: </b> Infection with Ebola virus (EBOV) causes a fulminant and often fatal hemorrhagic fever. In order to improve our understanding of EBOV pathogenesis and EBOV-host interactions we have examined the molecular features of EBOV infection in vivo. Using self-spotted cDNA microarrays, we analyzed genome-wide host expression patterns in sequential blood samples from nonhuman primates (NHP) infected with EBOV. <br> <p align="left"><b>Overall Design: </b> Ebola infection of non-human primates (cynomolgus macaques). We took sequential samples of peripheral blood mononuclear cells (PBMC) from 15 cynomolgus macaques infected intramuscularly with 1000 plaque forming units (PFUs) of EBOV, Zaire strain. Peripheral blood samples (2.5mL) were collected on days 1, 4, or 6 prior to infection, in order to define a robust baseline, and then on successive days after infection, until death (immediately prior to euthanasia). Animals were euthanized at days 1, 2, 3, 4, 5, and 6 postinfection. PBMC's were collected at days post-infection as noted, preserved in Trizol, Trizol-extracted total RNA, 1 round amplified (Ambion MessageAmp I), directly labeled by Cy5 incorporation during reverse transcription of amplified RNA. Each blood sample was hybridized versus a common reference. The same reference is used for all samples - Stratagene Universal Human Reference RNA, 1 round of amplification (Ambion MessageAmp I), directly labeled by Cy3 incorporation during reverse transcription of amplified reference RNA. Two to three biological replicates of pre-infection samples were taken for each animal, as well as two to nine biological replicates (from different animals) at each day post-infection. A total of 50 arrays, representing 15 animals is included in this dataset.
2008-03-11 | E-SMDB-4098 | biostudies-arrayexpress
Project description:Infection with Ebola virus (EBOV) causes a fulminant and often fatal hemorrhagic fever. In order to improve our understanding of EBOV pathogenesis and EBOV-host interactions we have examined the molecular features of EBOV infection in vivo. Using self-spotted cDNA microarrays, we analyzed genome-wide host expression patterns in sequential blood samples from nonhuman primates (NHP) infected with EBOV. A reference experiement design type is where all samples are compared to a common reference. Keywords: reference_design
2007-06-28 | GSE8317 | GEO
Project description:We performed transcriptomic analysis of a time course of Ebola virus (EBOV) iPSC-derived hepatocytes. Mock infected and EBOV infected hepatocytes were harvested 1, 2, 3, and 7 days post-infection for analysis. Hepatocytes were infected with EBOV at a multiplicity of infection of 10.
2022-09-01 | GSE184639 | GEO
Project description:Ebola virus can cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD),the mechanism of how this pathogenesis comes about is not well understood, It is assumed that miRNA may have important roles in virus infection response. To better understand the function of miRNA in EBOV infection disease, we undertook a miRNA profiling analysis using the whole blood of EBOV infection patients.
2023-12-31 | GSE83564 | GEO
Project description:Ebola (EBOV) virus causes severe and often lethal hemorrhagic fever in humans and nonhuman primates (NHP), and has been classified as a Category A bioweapon agent. There are currently no approved preventive vaccines or postexposure treatments for EBOV hemorrhagic fever. The mechanisms of EBOV pathogenesis are only partially understood, but the dysregulation of normal host immune responses (including destruction of lymphocytes, increases in levels of circulating proinflammatory cytokines, and development of coagulation abnormalities) is thought to play a major role. Accumulating evidence suggests that much of the observed pathology is not the direct result of virus-induced structural damage but rather is due to the release of soluble immune mediators from EBOV-infected cells. It is therefore essential to understand how the candidate therapeutic may be interrupting the disease process and/or targeting the infectious agent. Identification of effective treatment strategies may greatly benefit based on identification of molecular features of the host response to infection and treatment. In order to identify these gene signatures related to correlates of protection, we used a DNA microarray-based approach to compare the host genome-wide responses of EBOV-infected NHP responding to candidate therapeutics. With this approach, we have identified genes that appear to correlate with survival, including chemokine ligand 8 (CCL8/MCP-2), and revealed a subset of distinctly differently expressed genes that may provide possible targets for future diagnostics or therapeutics. These analyses will assist us in understanding the pathogenic mechanisms of EBOV infection as well as identify improved therapeutic strategies. Transcriptional analysis of global gene expression changes in Zaire Ebola Virus (ZEBOV)-infected rhesus macaques that were treated with either recombinant nematode anticoagulant protein c2 (rNAPc2) or recombinant human activated protein C (rhAPC). Animals were infected with 1000pfu ZEBOV, then subsequently treated with rNAPc2 or rhAPC. Four animals were left untreated for controls. Blood samples were taken at specified days post-infection and PBMCs were isolated from the samples and inactivated in TRIzol reagent. Total RNA was isolated from the samples, then linearly amplified and hybridized to a whole genome long-oligonucleotide microarray in a two color comparative format with a commercially available human reference RNA from Stratagene as a consistent control in dataset comparisons.
2010-11-30 | E-GEOD-24943 | biostudies-arrayexpress
Project description:Episodic Ebola virus (EBOV) outbreaks, such as the current one in West Africa, emphasize the critical need for novel antivirals against this highly pathogenic virus. Here, we demonstrate that interferon gamma (IFNγ) prevents morbidity and mortality associated with EBOV infection when administered to mice either 24 hours prior to or 2 hours following EBOV infection. Microarray studies with IFNγ-stimulated human macrophages identified novel interferon-stimulated genes (ISGs) that inhibit EBOV infection upon ectopic expression. IFNγ treatment reduced viral RNA levels in macrophages to a similar degree as cells treated with the protein synthesis inhibitor, cycloheximide, suggesting that IFNγ treatment inhibits genome replication. As IFNγ treatment robustly protects mice against EBOV infection, we propose that this FDA-approved drug may serve as a useful prophylactic or therapeutic strategy during EBOV outbreaks, contributing to the currently limited arsenal of filovirus antivirals.
2015-10-20 | GSE64995 | GEO
Project description:Ebola virus can cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD),the mechanism of how this pathogenesis comes about is not well understood, but it is well accepted that pathogenesis is significantly driven by a hyperactive immune response. To better understand the overall response to Ebola virus challenge, we undertook a transcriptomic analysis using the whole blood of EBOV infection patients.
2023-12-31 | GSE83563 | GEO
Project description:Episodic Ebola virus (EBOV) outbreaks, such as the current one in West Africa, emphasize the critical need for novel antivirals against this highly pathogenic virus. Here, we demonstrate that interferon gamma (IFNγ) prevents morbidity and mortality associated with EBOV infection when administered to mice either 24 hours prior to or 2 hours following EBOV infection. Microarray studies with IFNγ-stimulated human macrophages identified novel interferon-stimulated genes (ISGs) that inhibit EBOV infection upon ectopic expression. IFNγ treatment reduced viral RNA levels in macrophages to a similar degree as cells treated with the protein synthesis inhibitor, cycloheximide, suggesting that IFNγ treatment inhibits genome replication. As IFNγ treatment robustly protects mice against EBOV infection, we propose that this FDA-approved drug may serve as a useful prophylactic or therapeutic strategy during EBOV outbreaks, contributing to the currently limited arsenal of filovirus antivirals.
2015-10-20 | GSE64996 | GEO
Project description:Immune patterns in Ebola patients were characterized depending on the outcome of the illness. Non-healthy controls were compared to Ebola patients to define the specificity of the immune response against Ebola virus infection.
2019-05-09 | GSE122692 | GEO