Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA155619 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE36461: MiRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009) GSE36462: MiRNA profiling during infection with H7N7 influenza A virus (A/Ck/Germany/R28/H7N7/2003) GSE36553: mRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009) Refer to individual Series
2012-04-09 | E-GEOD-36555 | biostudies-arrayexpress
Project description:To further understand the roles of miRNA during influenza A virus infection, we performed miRNA profiling in human alveolar adenocarcinoma cell lines, A549 cells, infected with influenza A virus A/Beijing/501/2009(H1N1) and A/goose/Jilin/hb/2003(H5N1).
2017-03-22 | GSE96857 | GEO
Project description:To study miRNA expression profiles during highly pathogenic avian influenza virus infection, we conducted global miRNA expression profiling in human lung epithelial cells (A549) with or without H5N1 IAV infection. .
2014-09-25 | GSE61701 | GEO
Project description:The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, influenza A virus infected, influenza A virus infected in the presence of exogenous miR-141, miR-374b, miR-449b, miR-518b, and miR-1263, and influenza A virus infected in the presence of exogenous miR-147b, miR-190b, miR-199a, miR-512-5p, and miR-874 with 3 biological replicates for each group. Total RNA was purified from A549 cells that were mock infected or infected with influenza A virus (A/WSN/33, 5pfu/cell) alone or in the presence of miRNA mimics 10 hours after treatment.
2013-09-15 | E-GEOD-47937 | biostudies-arrayexpress
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
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
Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection. Control (mock-infected) samples: 12 (2 technical replicates, averaged), Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). The experiment was performed in six replicates.
2012-04-09 | E-GEOD-36553 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection.
2012-04-10 | GSE36462 | GEO
Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection.
2012-04-10 | GSE36461 | GEO