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Human Calu-3 cell transcriptome response to wild-type pandemic H1N1 (A/California/04/2009), natural isolate [mRNA]

ABSTRACT: The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in human Calu-3 cells infected with wild-type pandemic H1N1 (A/California/04/2009), natural isolate.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80697 | GEO | 2016/05/26

SECONDARY ACCESSION(S): PRJNA319728

REPOSITORIES: GEO

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Human Calu-3 cell transcriptome response to wild-type pandemic H1N1 (A/California/04/2009), natural isolate

Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in human Calu-3 cells infected with wild-type pandemic H1N1 (A/California/04/2009), natural isolate.

2016-05-07 | GSE80698 | GEO

Host Regulatory Network Response in Calu-3 cell Infection with A/CA/04/2009 Influenza virus

Project description:Differential Expression was determined in Calu-3 cells between mock infected and infection with A/CA/04/2009 Influenza virus at nime time points post infection.

2012-05-05 | GSE37571 | GEO

Host Regulatory Network Response in Calu-3 cell Infection with A/CA/04/2009 Influenza virus

Project description:Differential Expression was determined in Calu-3 cells between mock infected and infection with A/CA/04/2009 Influenza virus at nime time points post infection. Calu-3 cells were infected with A/CA/04/2009 Influenza virus at MOI of 3, samples were collected 0,3,7,12,18, 24, 30, 36 and 48 hpi. Expression profiles and DE genes were determined for all time points. There are 3 mock and infected replicates for each time point.

2012-05-04 | E-GEOD-37571 | biostudies-arrayexpress

ICL010 - Infection of Calu-3 cells with H1N1 influenza virus A/Netherlands/602/2009

2012-09-13 | GSE40844 | GEO

ICL010 - Infection of Calu-3 cells with H1N1 influenza virus A/Netherlands/602/2009

Project description:Differential expression was determined in Calu-3 cells between mock infected and infected with H1N1 influenza virus A/Netherlands/602/2009 at nine time points post-infection. As a comparison, cells were also infected with A/CA/04/2009 H1N1 influenza virus at 4 time points post-infection. Cells were infected at an MOI of 3.0. For the A/Netherlands/602/09-infected and mock-infected cells, samples were collected at 0, 3, 7, 12, 18, 24, 30, 36, and 48 hours post-infection (h.p.i.). For the A/California/04/2009-infected cells, samples were collected at 0, 12, 24, and 48 h.p.i. Samples were collected in triplicate.

2012-09-13 | E-GEOD-40844 | biostudies-arrayexpress

ICL002: Time course of Calu-3 cells infected with Influenza A/VN/1203/04

Project description:Purpose of experiment was to perform transcriptomics on Calu- 3 cells infected with Influenza A/VN/1203/04.

2011-11-01 | GSE33142 | GEO

ICL002: Time course of Calu-3 cells infected with Influenza A/VN/1203/04

Project description:Purpose of experiment was to perform transcriptomics on Calu- 3 cells infected with Influenza A/VN/1203/04. Calu-3 cells were infected with Influenza A/VN/1203/04, at MOI of 1.0. Cells samples were collected at 0, 3, 7, 12, 18, and 24 h post infection. Each infected sample was done in duplicate. (Duplicates are defined as 2 different wells, plated at the same time using the same cell stock for all replicates.)There is one time-matched mock for each time point from the same cell stock as rest of samples. Culture medium (the same as what the virus stock is in) was used for the mock infections. The NIAID Systems Virology Center

2011-11-01 | E-GEOD-33142 | biostudies-arrayexpress

Influenza A virus (A/California/04/2009(H1N1))

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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

Project description: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. Here, we compared the gene-expression response following infection of mice with A/CA/04/2009 (CA/04) or the virulent mouse-adapted strain (MA-CA/04). Microarray analysis revealed that increased pathogenicity of MA-CA/04 was associated with: (1) early and sustained inflammatory and interferon response that could be driven in part by interferon regulatory factors (IRFs) and increased NF-kappaB activation, as well as inhibition of the negative regulator TRIM24, (2) early and persistent infiltration of immune cells, including inflammatory macrophages, and (3) the absence of activation of lipid metabolism later in infection, that may be mediated by nuclear receptors inhibition, including PPARG, HNF1A and 4A, with pro-inflammatory consequences. Further investigation of these signatures in the host response to other H1N1 viruses of varied pathogenicity confirmed their general relevance for virulence of influenza virus and suggested that lung response to MA-CA/04 virus was similar to that following lethal H1N1 r1918 influenza virus. This study links for the first time differential activation of IRFs, nuclear receptors, and macrophage infiltration with influenza virulence in vivo.

2012-03-08 | GSE36328 | GEO

Mouse lung tissue transcriptome response to H1N1, H5N1, and mutants [mRNA]

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

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