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

ABSTRACT: 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(S): Gallus gallus

PROVIDER: GSE53930 | GEO | 2015/03/04

SECONDARY ACCESSION(S): PRJNA233995

REPOSITORIES: GEO

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

2015-03-04 | GSE53931 | GEO

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

Project description: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). Chickens were inoculated with CK10 or CK-PAX3 or mock-infected. At 24 hours post infection, lungs were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: CK10 (CK10-1,CK10-2,CK10-3), CK-PAX3 (CK-PAX3-1,CK-PAX3-2, CK-PAX3-3), Control (C-1, C-2, C-3).

2015-03-04 | E-GEOD-53931 | biostudies-arrayexpress

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

Project description: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). Chickens were inoculated with CK10 or CK-PAX3 or mock-infected. At 12 hours post infection, lungs were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: CK10 (CK10-1,CK10-2,CK10-3), CK-PAX3 (CK-PAX3-1,CK-PAX3-2, CK-PAX3-3), Control (C-1, C-2, C-3).

2015-03-04 | E-GEOD-53930 | biostudies-arrayexpress

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

2013-07-16 | GSE48890 | GEO

Gene expression data from lung of mice infected with H5N1 or H1N1 virus

2016-01-12 | GSE76719 | GEO

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)

Project description: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. We found that responses to the H7 subtype viruses were intermediate to those elicited by H5N1 and H1N1 early in infection, but that they evolved to resemble the H5N1 response as infection progressed. H5N1, H7N7 and H7N9 viruses were pathogenic in mice, and this pathogenicity correlated with increased cytokine response, decreased lipid metabolism and decreased coagulation signaling. This three-pronged signature has previously been observed in mice infected with pathogenic H1N1 strains such as the 1918 virus, indicating that it may be predictive of pathogenicity across multiple influenza strains.

2014-05-27 | GSE54048 | GEO

2014-05-27 | E-GEOD-54048 | biostudies-arrayexpress

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

Project description:Periodic outbreaks of highly pathogenic avian H5N1 influenza viruses and the current H1N1 pandemic highlight the need for a more detailed understanding of influenza virus pathogenesis. To investigate the host transcriptional response induced by pathogenic influenza viruses, we used a functional-genomics approach to compare gene expression profiles in lungs from wild-type 129S6/SvEv and interferon receptor (IFNR) knockout mice infected with either the fully reconstructed H1N1 1918 pandemic virus (1918) or the highly pathogenic avian H5N1 virus Vietnam/1203/04 (VN/1203). Eight- to 10-week-old female wild-type and IFNR1-/- mice (on a 129S6/SvEv background) were anesthetized by intraperitoneal injection of 0.2 ml of 2,2,2-tribromoethanol in tert-amylalcohol (Avertin; Sigma-Aldrich, Milwaukee, WI). Ten times the 50% lethal dose (LD50), 3.2 × 10^4 PFU (1918) or 7 × 10^3 PFU (VN/1203), in 50 μl of infectious virus diluted in phosphate-buffered saline (PBS) was inoculated intranasally (i.n.). Lung tissue was harvested for microarray analysis from infected animals at 1, 3, and 4 days post-innoculation. For RNA isolation, lungs were frozen in individual tubes and stored in solution D (4 M guanidinium thiocyanate, 25 mM sodium citrate, 0.5% sarcosyl, 0.1 M β-mercaptoethanol). Separate microarrays were run for each infected mouse. This included 2 animals/time point for 1918 virus-infected mice (24 animals total) or 3 animals/time point for VN/1203-infected mice (36 animals total). Lung tissue from three uninfected wild type 129S6/SvEv mice was collected as a mock control. Equal masses of total RNA from the lung tissue of the three mice were pooled prior to being run on microarray. Two-channel microarrays were used to determine gene expression in the lungs. For each individual infected lung, gene expression from an infected lung was compared to gene expression from the pooled RNA from the mock control.

2013-07-16 | E-GEOD-48890 | biostudies-arrayexpress

Gene expression data from lung of mice infected with H5N1 or H1N1 virus

Project description:To find the different host response during H5N1 and H1N1 infection, we have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed in mouse lungs infected by H5N1 and H1N1 virus. BALB/c mice were infected with live H5N1 virus , live H1N1 virus, or inactivated H5N1 virus or allantoic fluid (AF) for 24 h. Mice were intra-tracheally inoculated with 106 TCID50 of live H5N1 virus or an identical volume of inactivated H5N1 virus , 106 TCID50 of live H1N1 virus, or allantoic fluid (AF). After 24 hours, lungs were taken for RNA extraction and hybridization on Agilent microarrays.H5N1 and H1N1 virus induced gene expression in mouse was measured. This experiment was performed with 3 mice in each group.

2016-01-12 | E-GEOD-76719 | biostudies-arrayexpress

Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease. Calu-3 cells were infected with VN1203 influenza virus and profiled at 0, 3, 7, 12, 18, and 24 hours post infection. There are 3 mock and infected replicates for each time point.

2011-09-01 | E-GEOD-28166 | biostudies-arrayexpress

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