Ontology highlight
ABSTRACT:
PROVIDER: PRJNA637807 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11943010_1.fastq.gz | Fastqsanger.gz | |||
| SRR11943010_2.fastq.gz | Fastqsanger.gz | |||
| SRR11943011_1.fastq.gz | Fastqsanger.gz | |||
| SRR11943011_2.fastq.gz | Fastqsanger.gz | |||
| SRR11943012_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
Similar Datasets
Project description:The glucocorticoid-inducible protein annexin A1 has been shown to function as key-regulator of the resolution phase of inflammation but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Acute crescentic glomerulonephritis was induced in annexin A1 deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Intrinsic annexin A1 has a protective effect in reducing pro-inflammatory signals and infiltration of neutrophil granulocytes during crescentic GN. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.
2022-10-04 | GSE204873 | GEO
Project description:Influenza A virus, with the limited coding capacity of 10 to 14 proteins, requires the host cellular machinery for many aspects of its life cycle. Knowledge of these host cell requirements not only reveals molecular pathways exploited by the virus or triggered by the immune system, but also provides further targets for antiviral drug development. To uncover novel pathways and key targets of influenza infection, we assembled a large amount of data from 12 cell-based gene-expression studies of influenza infection for an integrative network analysis. We systematically identified differentially expressed genes and gene co-expression networks induced by influenza infection. We revealed the dedicator of cytokinesis 5 (DOCK5) played potentially an important role for influenza virus replication. CRISPR/Cas9 knockout of DOCK5 reduced influenza virus replication, indicating that DOCK5 is a key regulator for the viral life cycle. DOCK5’s targets determined by the DOCK5 knockout experiments strongly validated the predicted gene signatures and networks. This study systematically uncovered and validated fundamental patterns of molecular responses, intrinsic structures of gene co-regulation, and novel key targets in influenza virus infection.
2018-02-14 | GSE104168 | GEO
Project description:To investigate the effect of ANXA1, encoding annexin a1, on group 2 innate lymphoid cells (ILC2s), we downregulated the expression using lentiviral vector-based shRNA transfer and performed RNA-seq analysis.
2023-09-01 | GSE212517 | GEO
Project description:Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. However, the small proteins or micropeptides encoded by lncRNAs and their functions in viral infection remain largely unexplored. Here, we identified and characterized a small 110-amino acid protein named ORF6 encoded by the putative lncRNA PCBP1-AS1. Interestingly, both PCBP1-AS1 and ORF6 were significantly upregulated by influenza virus infection. Furthermore, we observed that they were markedly induced by type I interferon treatment. Overexpression of PCBP1-AS1 or ORF6 enhanced influenza virus replication. Conversely, knockdown of PCBP1-AS1 or knockout of ORF6 inhibited the viral production. In addition, loss-of-function experiment demonstrated that ORF6 is essential for PCBP1-AS1 to facilitate influenza virus replication. Importantly, the overexpression of ORF6 induced enhancement of autophagy by increasing the expression of ATG7, a gene encoding an essential effector enzyme for canonical autophagy. These findings reveal a lncRNA-derived small protein that is exploited by influenza virus, and provide new insights into the virus-host regulatory network.
2024-08-03 | GSE253139 | GEO
Project description:Influenza A virus is mainly transmitted through the respiratory route and can cause severe illness in humans. Proteins encoded by influenza A virus can interact with cellular factors and dysregulate host biological processes to facilitate viral replication and pathogenicity. The influenza viral PA protein is not only a subunit of influenza viral polymerase but also a virulence factor involved in pathogenicity during infection. To explore the role of the influenza virus PA protein in regulating host biological processes, we conducted immunoprecipitation and LC-MS/MS to globally identify cellular factors that interact with the PA proteins of the influenza A H1N1, 2009 pandemic H1N1, H3N2, and H7N9 viruses. The results demonstrated that proteins located in the mitochondrion, proteasome, and nucleus are associated with the PA protein. We further discovered that the PA protein is located in mitochondria by immunofluorescence and mitochondrial fractionation and that overexpression of the PA protein reduces mitochondrial respiration. In addition, our results revealed the interaction between PA and the mitochondrial matrix protein PYCR2 and the antiviral role of PYCR2 during influenza A virus replication. Moreover, we found that the PA protein could also trigger autophagy and disrupt mitochondrial homeostasis. Overall, our research revealed the impacts of the influenza A virus PA protein on mitochondrial function and autophagy.
2024-06-23 | PXD050585 | Pride
Project description:While a common symptom of influenza and coronavirus disease 2019 (COVID-19) is fever, its physiological role on host resistance to viral infection remains less clear. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C increase host resistance to viral pathogens including influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). High heat-exposed mice increase basal body temperature over 38 °C to enable more bile acids production in a gut microbiota-dependent manner. The gut microbiota-derived deoxycholic acid (DCA) and its plasma membrane-bound receptor Takeda G-protein-coupled receptor 5 (TGR5) signaling increase host resistance to influenza virus infection by suppressing virus replication and neutrophil-dependent tissue damage. Furthermore, the DCA and its nuclear farnesoid X receptor (FXR) agonist protect Syrian hamster from lethal SARS-CoV-2 infection. Moreover, we demonstrate that certain bile acids are reduced in the plasma of COVID-19 patients who developed moderate I/II disease compared with minor illness group. These findings uncover an unexpected mechanism by which virus-induced high fever increases host resistance to influenza virus and SARS-CoV-2 in a gut microbiota-dependent manner.
2023-01-24 | ST002476 | MetabolomicsWorkbench
Project description:While a common symptom of influenza and coronavirus disease 2019 (COVID-19) is fever, its physiological role on host resistance to viral infection remains less clear. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C increase host resistance to viral pathogens including influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). High heat-exposed mice increase basal body temperature over 38 °C to enable more bile acids production in a gut microbiota-dependent manner. The gut microbiota-derived deoxycholic acid (DCA) and its plasma membrane-bound receptor Takeda G-protein-coupled receptor 5 (TGR5) signaling increase host resistance to influenza virus infection by suppressing virus replication and neutrophil-dependent tissue damage. Furthermore, the DCA and its nuclear farnesoid X receptor (FXR) agonist protect Syrian hamster from lethal SARS-CoV-2 infection. Moreover, we demonstrate that certain bile acids are reduced in the plasma of COVID-19 patients who developed moderate I/II disease compared with minor illness group. These findings uncover an unexpected mechanism by which virus-induced high fever increases host resistance to influenza virus and SARS-CoV-2 in a gut microbiota-dependent manner.
2023-02-14 | ST002479 | MetabolomicsWorkbench
Project description:The pathogenesis of avian influenza A H5N1 virus in human has not been clearly elucidated. There have been increasing evidence suggesting a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. However, the role of aberrant innate immune response in human lungs infected by avian influenza H5N1 virus has not been explored and direct evidence for inappropriate innate responses in lungs of avian influenza H5N1 virus infected patients is lacking. In order to obtain evidences for the proposed role of aberrant innate immune response in avian influenza H5N1 virus pathogenesis in human, we analyzed expression profile of lung tissues from two fatal cases of avian influenza H5N1 virus infected patients in comparison to normal human lung using an expression microarray.
2010-06-16 | E-GEOD-22212 | biostudies-arrayexpress
Project description:CD47 is an ubiquitously expressed surface molecule that has a significant impact on immune responses. However, its role for antiviral immunity is not fully understood. We can show that CD47 has an inhibitory role in influenza virus defense, since CD47-deficient mice (CD47-/-) display an increased viral clearance during influenza virus infection. This effect is strongly associated with alveolar macrophages, yet the underlying mechanisms are unclear. Thus, to assess the precise impact of CD47 on antiviral action of alveolar macrophages, transcriptional analysis of ex vivo isolated alveolar macrophages from CD47-/- and WT mice were performed isolated 3dpi. Surprisingly, instead of classical antiviral mediators, an increased expression of both hemoglobin α and hemoglobin β was found in CD47 deficient compared to WT alveolar macrophages upon influenza A virus infection. Importantly, antiviral activity of hemoglobin was already shown for other viruses and thus, CD47 might limit influenza virus defense via the regulation of hemoglobin, which could act as a modulator of the antiviral immune response during the infection.
2022-12-09 | GSE201825 | GEO
Project description:Himanshu Manchanda, Nora Seidel, Andi Krumbholz, Andreas Sauerbrei, Michaela Schmidtke & Reinhard Guthke. Within-host influenza dynamics: a small-scale mathematical modeling approach. Biosystems 118 (2014).
The emergence of new influenza viruses like the pandemic H1N1 influenza A virus in 2009 (A(H1N1)pdm09) with unpredictable difficulties in vaccine coverage and established antiviral treatment protocols emphasizes the need of new murine models to prove the activity of novel antiviral compounds in vivo. The aim of the present study was to develop a small-scale mathematical model based on easily attainable experimental data to explain differences in influenza kinetics induced by different virus strains in mice. To develop a three-dimensional ordinary differential equation model of influenza dynamics, the following variables were included: (i) viral pathogenicity (P), (ii) antiviral immune defense (D), and (iii) inflammation due to pro-inflammatory response (I). Influenza virus-induced symptoms (clinical score S) in mice provided the basis for calculations of P and I. Both, mono- and biphasic course of mild to severe influenza induced by three clinical A(H1N1)pdm09 strains and one European swine H1N2 virus were comparatively and quantitatively studied by fitting the mathematical model to the experimental data. The model hypothesizes reasons for mild and severe influenza with mono- as well as biphasic course of disease. According to modeling results, the second peak of the biphasic course of infection is caused by inflammation. The parameters (i) maximum primary pathogenicity, (ii) viral infection rate, and (iii) rate of activation of the immune system represent most important parameters that quantitatively characterize the different pattern of virus-specific influenza kinetics.
2024-09-02 | BIOMD0000000712 | BioModels