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Influenza A virus strain:H7N9

ABSTRACT: Influenza A virus strain:H7N9 Genome sequencing

PROVIDER: PRJNA202283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR900260.fastq.gz	Fastqsanger.gz
	SRR900261.fastq.gz	Fastqsanger.gz
	SRR900262.fastq.gz	Fastqsanger.gz
	SRR900263.fastq.gz	Fastqsanger.gz
	SRR900264.fastq.gz	Fastqsanger.gz

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Pathogenesis of influenza A(H7N9) virus in aged non-human primates

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.

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Attenuation of A(H7N9) influenza virus infection in mice exposed to cigarette smoke

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Mouse lung tissue transcriptome response to a wild type infectious clone of H7N9 Influenza virus and mutant H7N9 viruses [microRNA]

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.

2015-05-16 | E-GEOD-68946 | biostudies-arrayexpress

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Transcriptomic expression profiles of SPF chicken-spleen infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4

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.

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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.

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Project description:The H7N9 influenza virus poses a significant threat to human health, and the mechanism by which it infects humans remains incompletely understood. Our investigation has unveiled significant insights into the role of glucosidase alpha, neutral C (ganc) gene in human H7N9 infections. Through whole genome sequencing (WGS), we identified five low-frequency functional and heterozygous variants of ganc strongly associated with human H7N9 infections compared to healthy controls. Furthermore, we observed a reduction in mRNA and protein expression of GANC following H7N9 virus infection in vitro and in vivo. Subsequent experiments involving GANC demonstrated promotion of H7N9 virus replication in a stable strain with GANC overexpression. Conversely, GANC knockdown exhibited the ability to restrict influenza A virus (IAV) replication, including H7N9, H9N2 and H1N1, both in vitro and in vivo. This inhibition was mediated by GANC's ability to promote the degradation of H7N9 hemagglutinin (HA). Moreover, we discovered that GANC knockdown facilitated the degradation of HA in a proteasome-dependent manner. The inhibition caused by GANC knockdown was mediated by promoting direct binding of HA with the proteasome 26S subunit, non-ATPase, 1 (PSMD1) and PSMD2. All the five variants in the ganc gene reduced its ability to promote H7N9 virus replication, and also diminished the levels of GANC-induced HA protein expression. Our findings revealed a novel mechanism by which GANC inhibited the proteasome-dependent degradation of HA to promote H7N9 virus replication. These results suggest that GANC may play an important role in IAV replication.

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Transcriptomic expression profiles of SPF chicken-lung infected with duck-origin H7N9 subtype avian influenza virus

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