Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA305099 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2973690_1.fastq.gz | Fastqsanger.gz | |||
| SRR2973690_2.fastq.gz | Fastqsanger.gz | |||
| SRR2973691_1.fastq.gz | Fastqsanger.gz | |||
| SRR2973691_2.fastq.gz | Fastqsanger.gz | |||
| SRR2973692_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:We report the whole genome sequencing of human bronchial cells infected with influenza A (PR/8/34) for 8 or 24 h. Examination influenza virus-specific human gene profiling at early or late stage of viral infection.
2016-08-24 | E-GEOD-75699 | biostudies-arrayexpress
Project description:Expression data from well-differentiated human bronchial epithelial cells infected with H1N1 Influenza isolates
| PRJNA210252 | ENA
Project description:Human rhinovirus and influenza virus infections of the upper airway lead to colds and the flu and can trigger exacerbations of lower airway diseases including asthma and chronic obstructive pulmonary disease. Despite modest advances in the diagnosis and treatment of infections by these viruses, novel diagnostic and therapeutic targets are still needed to differentiate between the cold and the flu, since the clinical course of influenza can be severe while that of rhinovirus is usually more mild. In our investigation of influenza and rhinovirus infection of human respiratory epithelial cells, we used a systems approach to identify the temporally changing patterns of host gene expression from these viruses. After infection of human bronchial epithelial cells (BEAS-2B) with rhinovirus, influenza virus or co-infection with both viruses, we studied the time-course of host gene expression changes over three days. From these data, we constructed a transcriptional regulatory network model that revealed shared and unique host responses to these viral infections such that after a lag of 4-8 hours, most cell host responses were similar for both viruses, while divergent host cell responses appeared after 24-48 hours. The similarities and differences in gene expression after epithelial infection of rhinovirus, influenza virus, or both viruses together revealed qualitative and quantitative differences in innate immune activation and regulation. These differences help explain the generally mild outcome of rhinovirus infections compared to influenza infections which can be much more severe. Human bronchial epithelial cells (BEAS-2B) were infected with rhinovirus, influenza virus or both viruses and RNAs were then profiled at 10 time points (2, 4, 6, 8, 12, 24, 26, 48, 60 and 72hrs)
2015-12-21 | E-GEOD-71766 | biostudies-arrayexpress
Project description:MicroRNA profiling of influenza A virus infected cells
| PRJNA208728 | ENA
Project description:Dynamic responses of primary human bronchial epithelial cells to influenza virus, viral RNA and interferon-beta
| PRJNA121751 | ENA
Project description:A. Esteban Hernandez-Vargas & Michael Meyer-Hermann. Innate Immune System Dynamics to Influenza Virus. IFAC Proceedings Volumes 45, 18 (2012).
The understanding of how influenza virus infection activates the immune system is crucial to designing prophylactic and therapeutic strategies against the infection. Nevertheless, the immune response to influenza virus infection is complex and remains largely unknown. In this paper we focus in the innate immune response to influenza virus using a mathematical model, based on interferon-induced resistance to infection of respiratory epithelial cells and the clearance of infected cells by natural killers. Simulation results show the importance of IFN-I to prevent new infections in epithelial cells and to stop the viral explosion during the first two days after infection. Nevertheless, natural killers response might be the most relevant for the first depletion in viral load due to the elimination of infected cells. Based on the reproductive number, the innate immune response is important to control the infection, although it would not be enough to clear completely the virus. The effective coordination between innate and adaptive immune response is essential for the virus eradication.
2024-09-02 | BIOMD0000000710 | BioModels
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Few studies have examined the local surface remodeling of primary human nasal epithelial cells (HNECs) during viral infection. Hence, the full range of upregulated adhesion molecules during respiratory viral infections that facilitate bacterial attachment and entry remain unknown. Accordingly, the current study provides a comprehensive view of HNEC responses to influenza virus pH1N1 infection, via global proteome profiling of uninfected (Mock, n = 4) and influenza-infected (Virus-only, n = 4) HNECs with isobaric tags using relative and absolute quantitation (iTRAQ) technique. A total of 3583 proteins were detected, 89 of which were significantly increased (52 proteins) or decreased (37 proteins) in the virus-infected HNECs compared to mock-infected controls (p < 0.05).
2024-05-08 | PXD042618 | Pride
Project description:The temporal response of primary human alveolar adenocarcinoma epithelial cells (A549) infected with H5N1 influenza virus and H9N2 influenza A viruswere evaluated using the proteomics approaches (2D-DIGE combined with MALDI-TOF-MS/MS) at 24 hours post of the infection .
2020-03-06 | PXD017921 |
Project description:We defined the major transcriptional responses in primary human bronchial epithelial cells (HBECs) after either infection with influenza or treatment with relevant ligands. We used four different strategies, each highlighting distinct aspects of the response. (1) cells were infected with the wild-type PR8 influenza virus that can mount a complete replicative cycle. (2) cells were transfected with viral RNA (‘vRNA’) isolated from influenza particles. This does not result in the production of viral proteins or particles and identifies the effect of RNA-sensing pathways (e.g., RIG-I.). (3) Cells were treated with interferon beta (IFNb), to distinguish the portion of the response which is mediated through Type I IFNs. (4) Cells were infected with a PR8 virus lacking the NS1 gene (‘DNS1’). The NS1 protein normally inhibits vRNA- or IFNb-induced pathways, and its deletion can reveal an expanded response to infection.
2010-03-30 | GSE19392 | GEO