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Global murine pulmonary response to highly and less virulent influenza A (H3N2) virus infections at 12, 48 and 96 h post-infection

ABSTRACT: Array analysis of total lung RNAs from female BALB/c mice collected at 12, 48 and 96 h post-infection with highly and less virulent influenza A (H3N2) viruses. Viruses (designated as LVI and HVI) were derived from influenza strain virus A/Aichi/2/68 (Aichi68). LVI is Aichi68 propagated in eggs, and HVI is mouse adapted Aichi68.

ORGANISM(S): Mus musculus

PROVIDER: GSE55994 | GEO | 2014/03/19

SECONDARY ACCESSION(S): PRJNA242120

REPOSITORIES: GEO

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Global murine pulmonary response to highly and less virulent influenza A (H3N2) virus infections at 12, 48 and 96 h post-infection

Project description:Array analysis of total lung RNAs from female BALB/c mice collected at 12, 48 and 96 h post-infection with highly and less virulent influenza A (H3N2) viruses. Viruses (designated as LVI and HVI) were derived from influenza strain virus A/Aichi/2/68 (Aichi68). LVI is Aichi68 propagated in eggs, and HVI is mouse adapted Aichi68. Infection: lung homogenate (mock), LVI and HVI; time of sample collection: 12, 48 and 96 h post-infection; two biological replicates for each group.

2014-03-19 | E-GEOD-55994 | biostudies-arrayexpress

Global murine neutrophil response to highly and less virulent influenza A (H3N2) virus infections at 3 and 9 h post-infection

Project description:Array analysis of total RNA obtained from MPRO neutrophils collected at 3 and 9 h post-infection with highly and less virulent influenza A (H3N2) viruses. Viruses (designated as LVI, HVI and MPI) were derived from influenza strain virus A/Aichi/2/68 (Aichi68). LVI is Aichi68 propagated in eggs, HVI is mouse adapted Aichi68, and MPI is HVI propagated in MDCK.

2014-03-19 | GSE55995 | GEO

Global murine neutrophil response to highly and less virulent influenza A (H3N2) virus infections at 3 and 9 h post-infection

2014-03-19 | E-GEOD-55995 | biostudies-arrayexpress

Gene expression in Calu-3 cells after influenza H3N2 and H11N9 infection

Project description:Airway epithelial cells are the initial site of infection with influenza viruses. The innate immune responses of airway epithelial cells to infection have the potential to limit virus replication and induce effective adaptive immune responses. However, relatively little is known about the importance of this innate anti-viral response to infection. Avian influenza viruses are a potential source of future pandemics, therefore it is critical to examine the effectiveness of the host anti-viral system to different influenza viruses. We used a human influenza (H3N2) and a low pathogenic avian influenza (H11N9) to assess and compare the anti-viral responses of bronchial epithelial cells (BECs). After infection, the H3N2 virus replicated more effectively than the H11N9 strain in BECs. This was not due to differential expression of different sialic acid residues on BECs but was attributed to the interference of the host anti-viral responses by H3N2. The H3N2 strain induced a delay in anti-viral signaling and impaired release of type I and type III interferons (IFNs) compared to the H11N9 virus. We then transfected the gene encoding for non-structural (NS) 1 protein into the BECs and the H3N2 NS1 induced a greater inhibition of anti-viral responses compared to the H11N9 NS1. While the low pathogenic avian influenza virus was capable of infecting BECs, the human influenza virus replicated more effectively than avian influenza virus in BECs and this may be at least in part due to a differential ability of the two NS1 proteins to inhibit anti-viral responses. This suggests that the subversion of human anti-viral responses may be an important requirement for influenza viruses to adapt to the human host and induce disease.

2009-12-19 | GSE19580 | GEO

Host microRNA molecular signatures associated with human H1N1 and H3N2 influenza A viruses

Project description:In this study, we performed a miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2).

2013-04-03 | GSE42003 | GEO

Transcriptomics profile of human bronchial epithelial cells exposed to influenza virus (H3N2) and ambient fine particles

Project description:Fine particulate matter (PM2.5) pollution remains a major threat to public health. As the physical barrier against inhaled air pollutants, airway epithelium is a primary target for PM2.5 and influenza viruses, two major environmental insults. Recent studies have shown that PM2.5 and influenza viruses may interact to aggravate airway inflammation, an essential event in the pathogenesis of diverse pulmonary diseases. Airway epithelium plays a critical role in lung health and disorders. Thus far, the mechanisms for the interactive effect of PM2.5 and the influenza virus on gene transcription of airway epithelial cells have not been fully uncovered. In this present pilot study, the transcriptome sequencing approach was introduced to identify responsive genes following individual and co-exposure to PM2.5 and influenza A (H3N2) viruses in a human bronchial epithelial cell line (BEAS-2B). Enrichment analysis revealed the function of differentially expressed genes (DEGs). Specifically, the DEGs enriched in the xenobiotic metabolism by the cytochrome P450 pathway were linked to PM2.5 exposure. In contrast, the DEGs enriched in environmental information processing and human diseases, such as viral protein interaction with cytokines and cytokine receptors and epithelial cell signaling in bacterial infection, were significantly related to H3N2 exposure. Meanwhile, this study found that co-exposure to PM2.5 and H3N2 may affect G protein-coupled receptors on the cell surface by modulating Ca2+. Thus, the results from this study provides insights into PM2.5- and influenza virus-induced airway inflammation and potential mechanisms

2023-11-15 | GSE244959 | GEO

Host microRNA molecular signatures associated with human H1N1 and H3N2 influenza A viruses

Project description:In this study, we performed a miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2). A549 cells were either mock-infected or infected at a multiplicity of infection (MOI) of 1 with H1N1 or H3N2 viruses, and total RNAs were isolated at 24 hours post-infection (hpi). An MOI of 1 was performed to ensure that 100% of the cells were infected at 24 hpi, a strategy that we have previously validated and used for a transcriptional profiling study of infected cells (Josset et al. , 2010). The purified RNAs were subjected to reverse transcription using a pool of miRNA RT primers (Human pool A v2.1, Applied Biosystems) and subsequently amplified and quantified by RT-qPCR in a TaqMan array MicroRNA card (Applied biosystems).

2013-04-03 | E-GEOD-42003 | biostudies-arrayexpress

Mouse lung transcriptome response to infection with H1N1, H3N2, and H5N1 influenza virus.

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

Influenza A virus H3N2

Project description:Deep sequencing of Influenza A/H3N2 Viruses Shed during 1 Year by an Immunocompromised Child

| PRJNA253584 | ENA

Host gene expression signatures of influenza A H1N1 and H3N2 virus infection in adults

Project description:Diagnosis of influenza A infection is currently based on clinical symptoms and pathogen detection. Use of host peripheral blood gene expression data to classify individuals with influenza A virus infection represents a novel approach to infection diagnosis We used microarrays to assay peripheral blood gene expression at baseline and every 8 hours for 7 days following intranasal influenza A H1N1 or H3N2 inoculation in healthy volunteers. We determined groups of coexpressed genes that classified symptomatic influenza infection. We then tested this gene expression classifier in patients with naturally acquired respiratory illness. We experimentally inoculated healthy volunteers with intranasal influenza A H1N1 and H3N2. Symptoms were documented and peripheral blood samples drawn into PAXgene RNA tubes for RNA isolation. We further enrolled patients presenting to the Emergency Department with naturally acquired respiratory illness, and documented symptoms and collected PAXgene RNA samples for RNA isolation.

2013-11-16 | E-GEOD-52428 | biostudies-arrayexpress

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