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Homo sapiens

ABSTRACT: A549 cell transcriptome responses to infection with H7N9 influenza virus

PROVIDER: PRJNA383550 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5458552_1.fastq.gz	Fastqsanger.gz
	SRR5458552_2.fastq.gz	Fastqsanger.gz
	SRR5458553_1.fastq.gz	Fastqsanger.gz
	SRR5458553_2.fastq.gz	Fastqsanger.gz
	SRR5458554_1.fastq.gz	Fastqsanger.gz

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A549 cell transcriptome responses to infection with H7N9 influenza 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.

2017-04-22 | GSE97949 | GEO

Characterizing the transcriptomic response of mice infected with A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), and A/Vietnam/1203/2004 (H5N1), and a pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1)

Project description:Modulating the host response is a promising approach to treating influenza, a virus whose pathogenesis is determined in part by the host response it elicits. Though the pathogenicity of emerging H7N9 influenza virus has been reported in several animal models, these studies have not included a detailed characterization of the host response following infection. To this end, we characterized the transcriptomic response of BALB/c mice infected with H7N9 (A/Anhui/1/2013) virus and compared it to the responses induced by H5N1 (A/Vietnam/1203/2004), H7N7 (A/Netherlands/219/2003) or H1N1 (A/Mexico/4482/2009) viruses. We found that responses to the H7 subtype viruses were intermediate to those elicited by H5N1 and H1N1 early in infection, but that they evolved to resemble the H5N1 response as infection progressed. H5N1, H7N7 and H7N9 viruses were pathogenic in mice, and this pathogenicity correlated with increased cytokine response, decreased lipid metabolism and decreased coagulation signaling. This three-pronged signature has previously been observed in mice infected with pathogenic H1N1 strains such as the 1918 virus, indicating that it may be predictive of pathogenicity across multiple influenza strains.

2014-05-27 | GSE54048 | GEO

2014-05-27 | E-GEOD-54048 | biostudies-arrayexpress

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.

2020-06-13 | GSE152406 | GEO

Homo sapiens

Project description:A549 human cells with influenza A virus infection

| PRJNA495615 | ENA

Transcriptomic characterization of the novel avian-origin influenza A (H7N9) virus: specific and intermediate host-response between avian (H5N1 and H7N7) and human (H3N2) viruses.

Project description:A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV.

2014-01-16 | GSE49840 | GEO

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.

2020-06-03 | GSE151662 | GEO

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

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.

2020-06-03 | GSE151661 | GEO

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

Project description:This study aims to determine how gene expression in the lung of mice is affected by cigarette smoking during infection with an H7N9 influenza virus.

2024-03-19 | GSE261627 | GEO

Differential expression data of BMDMs of mice infected with avian influenza influenza A (H7N9) viruses

Project description:To clarify the underlying mechanism that regulates the response of iron metabolism to influenza A virus infection, we analyzed gene expression profiles in mouse, bone marrow-derived macrophages (BMDMs) infected with H7N9 virus. In addition, We also analysed the chemokine, inflammation, innate-immunity, lipid-metabolism, transcription mRNA level by micrroarray. So, we gain the global transcriptional response in the BMDMs of mice infected with H7N9 virus.

2018-04-13 | GSE112964 | GEO

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