Project description:With the purpose to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus at 24 hours post-infection(hpi) and fowl adenovirus-4 at 48 dpi. The spleens of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 2426 differentially expressed genes were obtained in the duck-origin H7N9 subtype avian influenza virus group, including 913 up-regulated genes and 1513 down-regulated genes, and there were 1534 differentially expressed genes were obtained in the fowl adenovirus-4 group, including 632 up-regulated genes and 902 down-regulated genes.
Project description:In order to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus. The lungs of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus were collected and high throughout sequenced. Compared with the control group, there were 740 differentially expressed genes were obtained in infection group, including 602 up-regulated genes and 138 down-regulated genes. The analysis of the GO items showed that the differentially expressed genes were involved in immune responses and inflammatory responses. The results of KEGG analysis showed that 7 pathways were enriched significantly, in those the Toll-like pathway had 11 up-regulated genes, namely IL-6, TLR4, Pik3, IRF7, MD-2, IRF5, MYD88, CD86, STAT1, TLR2, and CCL4. There were 7 up-regulated genes in NOD-like receptor signaling pathway, which were IRF7, CTSB, P2RX7, CYBB, PSTPIP1, HSP90AA1, and NAMPT. In Toll-like signaling pathway，TLR4 was activated by MD-2 after viral infection, and then activated downstream IRF5. At the same time, the NLRP3 inflammasome also played an important role in the process of H7N9 virus infection.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Groups of 22-week-old C57BL/6 mice were infected with the H7N9 Influenza WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Infections were done at 10^4 PFU or time-matched mock infected. Time points were 1, 2, 4 and 7 d.p.i. There were 5 animals/dose/time point. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Groups of 22-week-old C57BL/6 mice were infected with the H7N9 Influenza WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Infections were done at 10^4 PFU or time-matched mock infected. Time points were 1, 2, 4 and 7 d.p.i. There were 5 animals/dose/time point. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
Project description:The objective of this study is to characterize the response to newly emerged, highly pathogenic H7N9 influenza virus isolated from human patients in 2013 in China. This study examines the pathogenesis of H7N9 influenza in cynomolgus macaques. The study compares lung lesions to adjacent right lower lobe lung tissue in animals necropsied at days 3 and 6 post-infection (n=4 animals/timepoint). 3-4 lesions from each animal were collected and equal amounts of pooled RNA from lesions from individual animals at each time point were used for microarray.
Project description:The avian influenza A(H7N9) virus has caused high mortality in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In this study, we employed non-human primates to evaluate the effect of aging on the pathogenicity of A(H7N9) virus. We observed that A(H7N9) virus infection of aged animals (defined as 20–26 years) caused more severe symptoms than infection of young animals (defined as 2 3 years). In aged animals, lung inflammation was weak and virus infection was sustained. Although cytokine and chemokine expression in the lungs of most aged animals was lower than that in the lungs of young animals, one aged animal showed dysregulated proinflammatory cytokine and chemokine production, resulting in it being euthanized. These results suggest that attenuated or dysregulated immune responses in aged animals are responsible for the severe symptoms observed among elderly patients infected with A(H7N9) virus.
Project description:mRNA-Seq analysis was used to profile the cellular transcriptome of A549 cells at multiple time points in response to infection with influenza H7N9.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus).
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus).
