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Transcriptome analysis of lungs from six different mouse strains after infection with highly pathogenic H5N1 influenza A virus

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE64800 | GEO | 2015/01/09

SECONDARY ACCESSION(S): PRJNA271891

REPOSITORIES: GEO

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Transcriptome analysis of lungs from six different mouse strains after infection with highly pathogenic H5N1 influenza A virus

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Transcriptome analysis of lungs from six different mouse strains after infection with highly pathogenic H5N1 influenza A virus [set 2]

Project description:Susceptible (DBA/2J, 129/SvImJ, A/J) and Resistant (SM/J, C57BL/6J, Balb/cJ) mouse strain were inoculated with a highly pathogenic H5N1 influenza A virus (A/Hong Kong/213/2003) for 72 hours or not infected (control animals). Differences in expression were analyzed and used to identify candidate genes and pathways that contributed to the difference in H5N1 pathogenesis in these two groups of mice. Female 6-8 weeks old animals were inoculated with H5N1 virus or not and 72 hours later the lungs were obtained and immediately homogenized in Trizol. The extracted RNA was submitted for Illumina Gene expression profiling.

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Transcriptome analysis of lungs from six different mouse strains after infection with highly pathogenic H5N1 influenza A virus [set 1]

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2015-01-09 | E-GEOD-64798 | biostudies-arrayexpress

Lung proteome analysis of highly pathogenic avian influenza virus (H5N1) infection progression in chicken

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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.

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Host regulatory network response to infection with highly pathogenic H5N1 avian influenza virus.

Project description:During the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, 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 system approach to identify and statistically validate signaling subnetworks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). Importantly, we validated a subset of transcripts from one subnetwork in both Calu-3 cells and mice. A more detailed examination of two subnetworks involved in the immune response and keratinization processes revealed potential novel mediators of HPAI H5N1 pathogenesis and host response signaling. Finally, we show how these results compare to those for a less virulent strain of influenza virus. 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 interventions for fatal HPAI H5N1 disease.

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

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?? T Cells Provide Protective Function in Highly Pathogenic Avian H5N1 Influenza A Virus Infection.

Project description:Given the high mortality rate (>50%) and potential danger of intrapersonal transmission, highly pathogenic avian influenza (HPAI) H5N1 epidemics still pose a significant threat to humans. ?? T cells, which participate on the front line of the host immune defense, demonstrate both innate, and adaptive characteristics in their immune response and have potent antiviral activity against various viruses. However, the roles of ?? T cells in HPAI H5N1 viral infection remain unclear. In this study, we found that ?? T cells provided a crucial protective function in the defense against HPAI H5N1 viral infection. HPAI H5N1 viruses could directly activate ?? T cells, leading to enhanced CD69 expression and IFN-? secretion. Importantly, we found that the trimer but not the monomer of HPAI H5N1 virus hemagglutinin (HA) proteins could directly activate ?? T cells. HA-induced ?? T cell activation was dependent on both sialic acid receptors and HA glycosylation, and this activation could be inhibited by the phosphatase calcineurin inhibitor cyclosporin A but not by the phosphatidylinositol 3-kinase (PI3-K) inhibitors wortmannin and LY294002. Our findings provide a further understanding the mechanism underlying ?? T cell-mediated innate and adoptive immune responses against HPAI H5N1 viral infection, which helps to develop novel therapeutic strategies for the treatment of H5N1 infection in the future.

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