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CircRNAs of A549 infected with H1N1/H7N9/H9N2 or PBS

ABSTRACT: circRNAs of A549 infected with H1N1/H7N9/H9N2 or PBS Raw sequence reads

PROVIDER: PRJNA868213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21002511_1.fastq.gz	Fastqsanger.gz
	SRR21002511_2.fastq.gz	Fastqsanger.gz
	SRR21002512_1.fastq.gz	Fastqsanger.gz
	SRR21002512_2.fastq.gz	Fastqsanger.gz
	SRR21002513_1.fastq.gz	Fastqsanger.gz

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Homo sapiens strain:H1N1/H7N9/H9N2 | isolate:H1N1/H7N9/H9N2 | breed:human | cultivar:iav

Project description:A549 infected with PBS/H1N1/H7N9/H9N2 circRNAs Raw sequence reads

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Homo sapiens strain:H1N1/H7N9/H9N2 | isolate:H1N1/H7N9/H9N2 | breed:human | cultivar:iav

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Transcriptional response of mice infected with H9N2 or H7N9

Project description:Transcriptional response of mice infected with H9N2 or H7N9

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Transcriptional response of mice infected with H9N2 or H7N9

Project description:Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses

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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.

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

H7N9 subtype

Project description:H7N9 Genome sequencing

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Glucosidase Alpha Neutral C Promotes Influenza Virus Replication by Inhibiting Proteosome-Dependent Degradation of Hemagglutinin

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.

2025-03-24 | GSE291573 | GEO

Human Calu-3 cell micro RNA transcriptome response to a wild type infectious clone of H7N9 Influenza virus and mutant H7N9 viruses

Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in human Calu-3 cells infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), and AH - NS1-103F/106M. Human Calu-3 cells were seeded at 1 x 10^6 cells per well on 6 well plates 2 days before infection. Prior to infection, washed cells 2 times with PBS, and then infected with a multiplicity of infection of 1. Infected samples were collected in quintuplet; time-matched mocks were collected in quintuplet in parallel with infected samples. Time points: 7 and 12 h post-infection

2015-05-20 | E-GEOD-69027 | biostudies-arrayexpress

Human Calu-3 cell transcriptome response to a wild type infectious clone of H7N9 Influenza virus and mutant H7N9 viruses

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