Project description:Whole-genome, time-course data was developed from the lungs of influenza infected mice to better characterize the dynamics of the host immune response during infection. Lung for microarray studies were obtained from female, five-week old C57BL/6Js infected with influenza viruses. Forty-two animals per group were inoculated with 10^5 PFU of A/Kawasaki/UTK-4/09 H1N1 virus [Kawasaki], A/California/04/09 (H1N1) virus (pH1N1) [SOIV], A/Vietnam/1203/04 H5N1 virus (H5N1), 10^3 PFU A/Vietnam/1203/04 H5N1 virus (H5N1) [VN1203] or mock-infected with PBS. Spanning the first week of the infections, three animals per infection group were sacrificed at 14 predetermined time points, lungs isolated and the homogenate was used to assess changes in genes expression over time and between infections.
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.
Project description:To delineate specific patterns of signaling networks activated by H5N1 we used a comparative systems biology approach analyzing gene expression in endothelial cells infected with three different human and avian influenza strains of high and low pathogenicity.
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 24 and 168 hours. Uninfected control animals were included. 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.
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.
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 24 and 168 hours. Uninfected control animals were included. 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 24 and 168 hours later the lungs were obtained and immediately homogenized in Trizol. The extracted RNA was submitted for Illumina Gene expression profiling.
Project description:Highly pathogenic influenza virus inhibit Inflammatory Responses in Monocytes via Activation of the Rar-Related Orphan Receptor Alpha (RORalpha). Low (PR8) and high pathogenic influenza viruses (FPV and H5N1) were used. Monocytes were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1)
