Ebola-infected non-human primates - PBMCs
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA101297
ORGANISM(S): Macaca fascicularis Homo sapiens
PROVIDER: GSE8317 | GEO | 2007/06/28
SECONDARY ACCESSION(S): PRJNA101297
REPOSITORIES: GEO
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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: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: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.
2010-11-30 | GSE24943 | GEO
Project description:Ebola virus disease (EVD) is a serious illness associated with 20-90% fatalities. EVD is characterized by robust virus replication and strong host inflammatory immune response. Analyzing the host immune response has increasingly involved multimodal approaches including transcriptomics to profile gene expression. We studied cynomolgus macaques exposed to Ebola virus (EBOV) Makona via different routes with the intent of comparing RNA-Seq to a NanoString nCounter codeset targeting 769 non-human primate (NHP) genes. RNA-Seq analysis of serial blood samples showed different routes led to the same overall transcriptional response seen in previously reported EBOV-exposed NHP studies. Similar profiles were observed using the NanoString codeset. Both platforms displayed a strong correlation in gene expression patterns, thus cross-validating the two methods. This included a strong induction of innate immune response genes at early time points post-infection, and neutrophil-associated genes at later time points. Using data generated from either platform, we could deploy a 41-gene classifier to cluster samples by EBOV infection status. Finally, NanoString and RNA-Seq identified changes in circulating immune cell populations that matched traditional hematology. Together, these results show the complementarity of RNA-Seq and NanoString for gene expression analysis, verifying host biomarkers of infection, and predicting changes in cell types.
2017-11-09 | GSE99463 | 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:The unprecedented 2013-16 outbreak of Ebola virus (EBOV) in West Africa resulted in over 11,300 human deaths. Host resistance to EBOV is thought to involve RIG-I-like receptor (RLR) signaling through the adaptor protein, mitochondrial antiviral signaling (MAVS), but role of RLR-MAVS in orchestrating anti-EBOV responses in vivo is not known. Here, we apply a systems approach to MAVS-deficient mice infected with either wild-type or mouse-adapted EBOV. MAVS controlled EBOV replication through expression of IFNα, IFN-stimulated genes, and regulation of inflammatory responses in the spleen, and prevented cell death in the liver, with macrophages implicated as a major cell-type influencing host resistance. A dominant role for RLR signaling in macrophages was confirmed following conditional deletion of MAVS in LysM+ myeloid cells. These findings reveal tissue-specific transcriptional pathways controlled by RLR signaling in resistance to EBOV, and suggest that EBOV adaptation to cause disease in mice is linked in part to increased antagonism of RLR-dependent signaling.
2016-12-31 | GSE83309 | GEO
Project description:Ebola virus (EBOV) causes epidemics with high mortality, yet remains understudied due to the challenge of experimentation in high-containment and outbreak settings. Here, we used single-cell transcriptomics and CyTOF-based single-cell protein quantification to characterize peripheral immune cells during EBOV infection in rhesus monkeys. We obtained 100,000 transcriptomes and 15,000,000 protein profiles, providing insight into pathogenesis: e.g., immature, proliferative monocyte-lineage cells with reduced antigen presentation capacity replace conventional monocyte subsets, while lymphocytes upregulate apoptosis genes and decline in abundance. By quantifying intracellular viral RNA, we identify molecular determinants of tropism among circulating immune cells and examine temporal dynamics in viral and host gene expression. Within infected cells, EBOV down-regulates STAT1 mRNA and interferon signaling, and up-regulates putative pro-viral genes (e.g., DYNLL1 and HSPA5), nominating pathways the virus manipulates for its replication. This study sheds light on EBOV tropism, replication dynamics, and elicited immune response, and provides a framework for characterizing host-virus interactions under maximum containment.
2020-09-23 | GSE158390 | GEO
Project description:We report comparative outcome-dependent transcriptional profiles from spleen and liver from Collaborative Cross mice infected with mouse-adapted Ebola virus (MA-EBOV).
2019-12-01 | GSE130629 | GEO
Project description:Ebola virus (EBOV) causes epidemics with high mortality, yet remains understudied due to the challenge of experimentation in high-containment and outbreak settings. Here, we used single-cell transcriptomics and CyTOF-based single-cell protein quantification to characterize peripheral immune cells during EBOV infection in rhesus monkeys. We obtained 100,000 transcriptomes and 15,000,000 protein profiles, providing insight into pathogenesis: e.g., immature, proliferative monocyte-lineage cells with reduced antigen presentation capacity replace conventional monocyte subsets, while lymphocytes upregulate apoptosis genes and decline in abundance. By quantifying intracellular viral RNA, we identify molecular determinants of tropism among circulating immune cells and examine temporal dynamics in viral and host gene expression. Within infected cells, EBOV down-regulates STAT1 mRNA and interferon signaling, and up-regulates putative pro-viral genes (e.g., DYNLL1 and HSPA5), nominating pathways the virus manipulates for its replication. This study sheds light on EBOV tropism, replication dynamics, and elicited immune response, and provides a framework for characterizing host-virus interactions under maximum containment.
2020-09-23 | GSE158442 | GEO