Gene expression data from lung of mice infected with H5N1 or H1N1 virus
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76719 | GEO | 2016/01/12
SECONDARY ACCESSION(S): PRJNA308453
REPOSITORIES: GEO
Similar Datasets
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
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. Groups of 6- to 8-week-old BALB/c mice were infected with either A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), A/Vietnam/1203/2004 (H5N1), or pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1). Infections were done at 10^5 PFU or time-matched mock infected. Time points were 1, 3 and 5 d.p.i. There were 4-5 infected and 3 mock infected animals/time point. Lung samples were collected for virus load and transcriptional analysis. Weight loss and animal survival were also monitored.
2014-05-27 | E-GEOD-54048 | biostudies-arrayexpress
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
Project description:Background: Influenza A virus (IAV) is a segmented negative-stranded RNA virus that brings a potentially serious threat to public health and animal husbandry. Mast cells play an important role in both the inherent and adaptive immune response. Previous studies have indicated that mast cells support the productive replication of H1N1, H5N1, and H7N2. To date, the distinct molecular mechanism behind the pathogenesis in mast cells among the three different viruses has been poorly understood. Methods: We investigated the genomic profiles in detail and the dynamic change of genomes regulated by different subtypes of IAV in mouse mast cells using microassays in order to the distinct molecular mechanism behind the pathogenesis in mast cells among the three different viruses. Mouse mast cells (P815) were infected at a multiplicity of infection of 1 (infectious viruses/cell) and incubated for 12 hr before collection of total RNA and microarray anlaysis using the Affymetrix platforms. Any two of the three IAV-infected groups were compared to detect genomic distinct. Based on the results of microassays, the further verification was performed by real-time PCR and western blotting. Here, the mRNA levels of 5-HT, PKG and HIF-1 in P815 cells following H1N1, H5N1 and H7N2 infection were determined by real-time PCR. The protein levels of exosomes in P815 cells following H1N1, H5N1 and H7N2 infection were detected by western blotting. Results: Compared with any two of the three IAV-infected groups, much more differentially expressed genes (DEGs), cellular functions and signaling pathways were confirmd in H1N1 or H7N2 group, and H7N2 group showed the highest levels. However, few DEGs were detected as well as various cellular functions and signaling pathways were dramatically suppressed in H5N1 group. With an in-depth study on H1N1 and H7N2 group, we demonstrated the 5-HT signaling pathway and cGMP/PKG signaling pathway terms were enriched in P815 cells infected by H1N1 while HIF-1 signaling pathway terms were enriched in P815 cells infected by H7N2 virus. Furthermore, RT-qPCR results also showed significantly increased mRNA of 5-HT and PKG in H1N1-infected P815 cells as well as HIF-1 in H7N2-infected P815 cells. Besides, exosomes were highly secreted from H1N1-infected or H7N2-infected P815 cells. Conclusions: H1N1 and H7N2 viruses could result in a variety of DEGs in mast cells and activate various cellular functions and signaling pathways while H5N1 virus cause the few DEGs in mast cells as well as suppression of cellular functions and signaling pathways. Furthermore, 5-HT signaling pathway and cGMP/PKG signaling pathway were preferentially activated in P815 cells infected by H1N1 while HIF-1 signaling pathway were preferentially activated in P815 cells infected by H7N2 virus. In addition, exosomes were also preferentially secreted from H1N1-infected or H7N2-infected P815 cells that are potentially pivotal in innate immunity to fight IAV infection. The study provides novel information and insight into the distinct of molecular mechanism of H1N1, H5N1 and H7N2 viruses in mast cells from the perspective of genomic profiles.
2019-04-12 | GSE129623 | GEO
Project description:Analysis of lung samples from mice infected with a severe H5N1 influenza virus (VN/1203/04/H5N1) or a mild H1N1 influenza virus (NYMC-X-179A) on day 3 and day 5 post-infection. Uninfected controls were used for comparison.
2016-12-20 | GSE70882 | GEO
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Vietnam/1203/2004 (H5N1; 'VN1203'), VN1203-NS1trunc124, and WT A/California/04/2009 (H1N1; 'CA04'). Groups of 22-week-old C57BL/6 mice were infected with WT A/Vietnam/1203/2004 (H5N1; 'VN1203'), VN12013-PB2-627E, VN1203-NS1trunc124, and WT A/California/04/2009 (H1N1; 'CA04').Infections were done at 176 PFU/mouse for VN1203, 1100 PFU/mouse for VN1203-NS1trunc124, and 10^4 PFU/mouse for CA04. Time points were 1, 2, 4, and 7 d.p.i. There were 5 mice for all infection groups and 3 mice for all mock groups. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
2015-06-18 | E-GEOD-69945 | biostudies-arrayexpress
Project description:The cellular transcriptome of C57BL/6 mouse lungs was profiled by mRNA-Seq analysis at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53. A/Wyoming/03/03 (H3N2) influenza virus replicates poorly in mice and lung tissue collected from mice inoculated with this virus did not carry viral loads detectable by plaque assay.
2017-05-05 | GSE98527 | GEO
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Vietnam/1203/2004 (H5N1; 'VN1203'), VN12013-PB2-627E, VN1203-NS1trunc124, and WT A/California/04/2009 (H1N1; 'CA04'). Groups of 22-week-old C57BL/6 mice were infected with WT A/Vietnam/1203/2004 (H5N1; 'VN1203'), VN12013-PB2-627E, VN1203-NS1trunc124, and WT A/California/04/2009 (H1N1; 'CA04').Infections were done at 176 PFU/mouse for VN1203, 70 PFU/mouse for VN1203-PB2-627E, 1100 PFU/mouse for VN1203-NS1trunc124, and 10^4 PFU/mouse for CA04. Time points were 1, 2, 4, and 7 d.p.i. There were 8 mice for all infection groups and 5 mice for all mock groups. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
2015-06-18 | E-GEOD-69944 | biostudies-arrayexpress
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Vietnam/1203/2004 (H5N1; 'VN1203'), VN1203-NS1trunc124, and WT A/California/04/2009 (H1N1; 'CA04').
2015-06-18 | GSE69945 | GEO
Project description:Human tracheobronchial epithelial (HTBE) cells are considered to serve as a good correlate of influenza virus infection in the human respiratory tract. mRNA-Seq analysis was used to profile the cellular transcriptome of HTBE cells at multiple time points in response to infection with influenza A/California/04/09 (H1N1), A/Wyoming/03/03 (H3N2), and A/Vietnam/1203/04 (H5N1) HALo virus. The Influenza A/Vietnam/1203/04 (H5N1) HALo mutant virus is an attenuated H5N1 virus generated from wild-type Influenza A/Vietnam/1203/04 (H5N1) virus as described in Steel, J., et al. J Virol. 2009 Feb; 83(4):1742-53.
2016-10-27 | GSE89008 | GEO