Similar studies for GEO DataSets (Select 200036328) - GEO DataSets

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Items: 20

Select item 2000363281.

IM002, IM009 - Implication of inflammatory macrophages, nuclear receptors and interferon regulatory factors in increased virulence of pandemic 2009 H1N1 influenza A virus after host adaptation

(Submitter supplied) While pandemic 2009 H1N1 influenza A viruses were responsible for numerous severe infections in humans, these viruses do not typically cause corresponding severe disease in mammalian models. However, the generation of a virulent 2009 H1N1 virus following serial lung passage in mice has allowed for the modeling of human lung pathology in this species. Genetic determinants of mouse-adapted 2009 H1N1 viral pathogenicity have been identified, but the molecular and signaling characteristics of the host response following infection with this adapted virus have not been described. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL7202
64 Samples

Download data: TXT

Series

Accession:: GSE36328

ID:: 200036328

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Select item 2000540482.

Characterizing the transcriptomic response of mice infected with A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), and A/Vietnam/1203/2004 (H5N1), and a pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1)

(Submitter supplied) Modulating the host response is a promising approach to treating influenza, a virus whose pathogenesis is determined in part by the host response it elicits. Though the pathogenicity of emerging H7N9 influenza virus has been reported in several animal models, these studies have not included a detailed characterization of the host response following infection. To this end, we characterized the transcriptomic response of BALB/c mice infected with H7N9 (A/Anhui/1/2013) virus and compared it to the responses induced by H5N1 (A/Vietnam/1203/2004), H7N7 (A/Netherlands/219/2003) or H1N1 (A/Mexico/4482/2009) viruses. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL7202
68 Samples

Download data: TXT

Series

Accession:: GSE54048

ID:: 200054048

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Select item 2000535233.

Comparative Time Course Profiles of Phthalate Stereoisomers in Mice

(Submitter supplied) Analysis of gene expression level in a mouse tumorigenic phthalate, DEHP vs non-tumorigenic DNOP. The hypothesis tested in the present study was to identify early key event thresholds related to tumor outcomes in a two-year carcinogenicity bioassay. Our results highlight marked differences in the toxicity profiles of structurally similar phthalates and demonstrate quantitative relationships between early bioindicators and later tumor outcomes.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL15097
16 Samples

Download data: TXT

Series

Accession:: GSE53523

ID:: 200053523

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Select item 2000498404.

Transcriptomic characterization of the novel avian-origin influenza A (H7N9) virus: specific and intermediate host-response between avian (H5N1 and H7N7) and human (H3N2) viruses.

(Submitter supplied) A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL17077
78 Samples

Download data: TXT

Series

Accession:: GSE49840

ID:: 200049840

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Select item 2000489765.

Cynomolgus macaque model of H7N9 influenza infection

(Submitter supplied) The objective of this study is to characterize the response to newly emerged, highly pathogenic H7N9 influenza virus isolated from human patients in 2013 in China. This study examines the pathogenesis of H7N9 influenza in cynomolgus macaques. The study compares lung lesions to adjacent right lower lobe lung tissue in animals necropsied at days 3 and 6 post-infection (n=4 animals/timepoint). 3-4 lesions from each animal were collected and equal amounts of pooled RNA from lesions from individual animals at each time point were used for microarray.

Organism:: Macaca fascicularis; Macaca mulatta

Type:: Expression profiling by array

Platform:: GPL17465
24 Samples

Download data: TXT

Series

Accession:: GSE48976

ID:: 200048976

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Select item 2000705026.

The 1918 PB2 protein, not HA, enhances the virulence of an avian influenza virus closely related to the 1918 pandemic virus through the inhibition of wnt signaling.

(Submitter supplied) The purpose of this experiment was to understand the pathogenic role of individual 1918 genes on the host response to the 1918 pandemic influenza virus. We examined reassortant avian viruses nearly identical to the pandemic 1918 virus (1918-like avian virus) carrying either the 1918 HA or PB2 gene. Both genes enhanced 1918-like avian virus replication, but only the mammalian host adaptation of the 1918-like avian virus through reassortment of the 1918 PB2 led to increased lethality in mice. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL7202
66 Samples

Download data: TXT

Series

Accession:: GSE70502

ID:: 200070502

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Select item 2000277027.

Highly Pathogenic Avian Influenza Viruses Avoid Effective Inflammatory Response of Human Macrophages

(Submitter supplied) Macrophages were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1). To our surprise a genome-wide comparative systems biology approach revealed that in contrast PR8 infections with HPAIV H5N1 and FPV result in a reduced immune response of human macrophages contradicting a primary role of this cell type for the cytokine storm. Our data point to a viral strategy of HPAIV to bypass a major amplifier of the initial local inflammatory response thereby hampering antiviral effector mechanisms and facilitating virus spreading and systemic disease.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL571
12 Samples

Download data: CEL, CHP

Series

Accession:: GSE27702

ID:: 200027702

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Select item 2000188168.

Expression data of influenza A infected human macrophages

(Submitter supplied) Human disease caused by highly pathogenic avian influenza (HPAI) H5N1 can lead to a rapidly progressive viral pneumonia leading to acute respiratory distress syndrome. There is increasing evidence suggests a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. The key target cells for the virus in the lung are the alveolar epithelium and alveolar macrophages, and previous data has shown that compared to seasonal human influenza viruses, equivalent infecting doses of H5N1 viruses markedly up-regulate pro-inflammatory cytokines in both primary cell types in vitro. more...

Organism:: Homo sapiens

Type:: Expression profiling by array

Dataset:: GDS3595
Platform:: GPL6244
27 Samples

Download data: CEL, CHP

Series

Accession:: GSE18816

ID:: 200018816

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Select item 35959.

Macrophage response to H1N1 and H5N1 influenza viral infections

Analysis of macrophages at 1, 3, and 6 hours post-infection with H1N1 or H5N1 viruses in vitro. The avian H5N1 virus is highly pathogenic, while the swine H1N1 virus is less so. Alveolar macrophages are targets of H5N1. Results provide insight into the host response to H1N1 and H5N1 infections.

Organism:: Homo sapiens

Type:: Expression profiling by array, transformed count, 3 individual, 3 infection, 3 time sets

Platform:: GPL6244
Series:: GSE18816
27 Samples

Download data: CEL, CHP

DataSet

Accession:: GDS3595

ID:: 3595

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 20005393210.

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Gallus gallus

Type:: Expression profiling by array

Platform:: GPL3213
18 Samples

Download data: CEL

Series

Accession:: GSE53932

ID:: 200053932

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Select item 20005393111.

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [24 hours post infection]

(Submitter supplied) Recently, a novel protein in the influenza virus segment 3 has been identified, namely PA-X. This small protein has been reported to play a role in modulating host response of the 1918 H1N1 pandemic virus-infected mice. However, poteinal role of this protein in the pathogenicity and regulating host response of the highly pathogenic H5N1 virus in a chicken animal model is completely unknown. We used microarray analysis to evaluate the global transcriptional response in the lungs of the chickens infected with the parental strain (CK10) and PA-X deficiency mutant strain (CK-PAX3).

Organism:: Gallus gallus

Type:: Expression profiling by array

Platform:: GPL3213
9 Samples

Download data: CEL

Series

Accession:: GSE53931

ID:: 200053931

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Select item 20005393012.

Expression data of lungs from chickens infected with different H5N1 Avian Influenza Viruses [12 hours post infection]

Organism:: Gallus gallus

Type:: Expression profiling by array

Platform:: GPL3213
9 Samples

Download data: CEL

Series

Accession:: GSE53930

ID:: 200053930

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Select item 20003152413.

Host cells infected by various types of viruses

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens; Canis lupus familiaris; Gallus gallus; Mus musculus

Type:: Expression profiling by array

4 related Platforms
228 Samples

Download data: CEL, CHP

Series

Accession:: GSE31524

ID:: 200031524

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Select item 20003151814.

Host cell gene expression in Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells at 2, 4, 6, 8 and 10 hours post infection

(Submitter supplied) We used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1))