E-MTAB-6192
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6192 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-6192-analysis-methods.tsv | Tabular | |||
| E-MTAB-6192-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-6192-configuration.xml | Xml | |||
| E-MTAB-6192-percentile-ranks.tsv | Tabular | |||
| E-MTAB-6192.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 70 |
Similar Datasets
Project description:Fribourg2014 - Dynamics of viral antagonism and innate immune response (H1N1 influenza A virus - NC/99)
The dynamics of the interplay between the viral antagonism and the innate immune response has been studied using modelling approaches. The responses of human monocyte-derived dendritic cells infected by two influenza A H1N1 strains (the pandemic swine-origin A/California/4/2009 (Cal/09) and the seasonal A/New Caledonia/20/1999 (NC/99)) that have different clinical outcomes have been modelled. From the time course gene expression measurements of a set of selected genes, the dynamic features of viral antagonism and innate immune response are extracted. It is found that the strength and the time scale of action of viral antagonism is significantly different between the two viruses. This model describes the viral infection by seasonal NC/99.
This model is described in the article:
Model of influenza A virus infection: Dynamics of viral antagonism and innate immune response.
Fribourg M, Hartmann B, Schmolke M, Marjanovic N, Albrecht RA, García-Sastre A, Sealfon SC, Jayaprakash C, Hayot F.
J Theor Biol. 2014 Mar 2;351C:47-57.
Abstract:
Viral antagonism of host responses is an essential component of virus pathogenicity. The study of the interplay between immune response and viral antagonism is challenging due to the involvement of many processes acting at multiple time scales. Here we develop an ordinary differential equation model to investigate the early, experimentally measured, responses of human monocyte-derived dendritic cells to infection by two H1N1 influenza A viruses of different clinical outcomes: pandemic A/California/4/2009 and seasonal A/New Caledonia/20/1999. Our results reveal how the strength of virus antagonism, and the time scale over which it acts to thwart the innate immune response, differs significantly between the two viruses, as is made clear by their impact on the temporal behavior of a number of measured genes. The model thus sheds light on the mechanisms that underlie the variability of innate immune responses to different H1N1 viruses.
This model is hosted on BioModels Database and identified
by: MODEL1403310001.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication for more information.
2024-09-02 | BIOMD0000000529 | BioModels
Project description:Fribourg2014 - Dynamics of viral antagonism and innate immune response (H1N1 influenza A virus - Cal/09)
The dynamics of the interplay between the viral antagonism and the innate immune response has been studied using modelling approaches. The responses of human monocyte-derived dendritic cells infected by two influenza A H1N1 strains (the pandemic swine-origin A/California/4/2009 (Cal/09) and the seasonal A/New Caledonia/20/1999 (NC/99)) that have different clinical outcomes have been modelled. From the time course gene expression measurements of a set of selected genes, the dynamic features of viral antagonism and innate immune response are extracted. It is found that the strength and the time scale of action of viral antagonism is significantly different between the two viruses. This model describes the viral infection by seasonal Cal/09.
This model is described in the article:
Model of influenza A virus infection: Dynamics of viral antagonism and innate immune response.
Fribourg M, Hartmann B, Schmolke M, Marjanovic N, Albrecht RA, García-Sastre A, Sealfon SC, Jayaprakash C, Hayot F.
J Theor Biol. 2014 Mar 2;351C:47-57.
Abstract:
Viral antagonism of host responses is an essential component of virus pathogenicity. The study of the interplay between immune response and viral antagonism is challenging due to the involvement of many processes acting at multiple time scales. Here we develop an ordinary differential equation model to investigate the early, experimentally measured, responses of human monocyte-derived dendritic cells to infection by two H1N1 influenza A viruses of different clinical outcomes: pandemic A/California/4/2009 and seasonal A/New Caledonia/20/1999. Our results reveal how the strength of virus antagonism, and the time scale over which it acts to thwart the innate immune response, differs significantly between the two viruses, as is made clear by their impact on the temporal behavior of a number of measured genes. The model thus sheds light on the mechanisms that underlie the variability of innate immune responses to different H1N1 viruses.
This model is hosted on BioModels Database and identified
by: MODEL1403310002.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication for more information.
2024-09-02 | BIOMD0000000528 | BioModels
Project description:Transcriptome analysis of different populations of human monocyte-derived myeloid cells: Autologous Tolerogenic Dendritic Cells (ATDCs), Monocyte-derived Dendritic Cells (MoDCs) and Monocyte-derived Macrophages (MoMacro)
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Project description:Dengue is one of the most important arboviruses in the world, with 2.5 billion people living in areas under risk to contagious. Mosquitos from Aedes genus is the transmission vector of viral particles. The virus genome inserted in these particles is formed by a single strain of RNA molecule which codifies three structural (C, prM, and E proteins) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5). The NS3 protein is involved in viral replication, with helicase (NS3hell) and protease functions. Once inoculated, the primary target for dengue virus (DV) infection is the Dendritic Cells (DC) in the site of mosquitos bit. The Dendritic Cells is the most efficient antigen-presenting cell holding the connection of innate immune system with adaptive immune system. In this study we examined the response of human monocyte-derived DC (mdDCs) DV-infected with two different strains how contain a single point mutation in L435S or L480S position of NS3hell protein, named vBAC-NS3435 and vBAC-NS3480 respectively. The analysis of these results demonstrated that the mutated strains can infect more efficiently the mdDCs compared with parental virus (vBACDV1) with more percentage of cells infected, replication and virus progeny. Infections of mdDCs with mutated DV can induce a differentiated response in gene profile of theses cells, with up-regulation of IFN Signaling and PRR canonical pathways. In the PRR pathway the expression of TLR3 and TLR7 was determined and these seem to be the route of sensing of the ssRNA-virus for the infected mdDCs. These sensing of the DV by mdDCs is translated in production of Type I IFN. The Type I IFN production was more important in mdDC DV-infected with mutated strains compared with parental strain. However, the enhanced levels of Type I IFN production were unable to prevent mdDCs infection by mutated strains. A18:J192replication. In the absence of Type I IFN action, the percentage of mdDCs infected by mutated strains was significantly incremented compared with DV-infection in the presence of Type I IFN, demonstrating that the Type I IFN action was effective but not sufficient to prevent viral replication of mutated strains. The single point mutation in NS3hell protein of vBAC-NS3435 and vBAC-NS3480 are sufficient to enhance the replication and bypass the Type I IFN action. All these results together can demonstrated that the single point mutation in a NS3hel protein of DV can subvert the normal replication pathway of the virus and these change can’t by controlled by human mdDC production of Type I IFN.
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Project description:In vitro experiment of stimulation of monocyte-derived dendritic cells with Saccaromyces cerevisiae in exponential growth phase. This experiment was performed to verify the comparability of microarray experiments using a pathway based logic (Beltrame et al., PLoS 2009) by comparing the analysis of this sample with other seven public data sets on monocyte-derived dendritic cells subjected to different stimuli retrieved from GEO Keywords: Case-control, transcriptional profiling, dendritic cells
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Project description:WGS and WGBS data from monocyte-derived macrophages that were infected with Influenza A virus strain PR8WT, or a matching non-infected control.
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Project description:In vitro experiment of stimulation of monocyte-derived dendritic cells with Saccaromyces cerevisiae in exponential growth phase. This experiment was performed to verify the comparability of microarray experiments using a pathway based logic (Beltrame et al., PLoS 2009) by comparing the analysis of this sample with other seven public data sets on monocyte-derived dendritic cells subjected to different stimuli retrieved from GEO Keywords: Case-control, transcriptional profiling, dendritic cells A case-control experiment consisting of 3 case samples (stimulated dendritic cells) compared to 3 paired (from the same donor) samples
2010-05-14 | E-GEOD-13901 | biostudies-arrayexpress
Project description:The purpose is to obtain samples for mRNA analysis in primary mouse myeloid dendritic cells infected with wild type West Nile virus (WNVMT) and mutant virus (WNVE218A).
2015-11-04 | GSE74628 | GEO
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