Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA806911 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transmission dynamics of AIV at the wild bird-poultry-human interfaces in Egyptian LBM
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Project description:Dynamics of human/poultry LBM interfaces in Bangladesh
| PRJNA806923 | ENA
Project description:Avian influenza caused significant damages to the poultry industry, efforts have been made to reveal the disease mechanisms as well as mechanisms of disease resistance. Here, by investigating two chicken breeds with distinct responses to avian influenza virus (AIV), Leghorn GB2 and Fayoumi M43, we compared their differences in genome, methylation and transcriptome. Except for MX1 involved direct acting antiviral mechanism, we found that in both methylation and transcriptome levels the more AIV resistant breed Fayoumi showed less variations compared to White Leghorn after AIV challenging. Fayoumi also showed better consistency between the changes in methylation and changes in transcriptome level. Our results suggested a homeostasis hypothesis of avian influenza resistance, with Fayoumi better maintaining homeostasis both in epigenetic and gene expression levels.
2019-03-15 | GSE128053 | GEO
Project description:Pathogens that cause respiratory diseases in poultry are very complicated, and co-infections with multiple pathogens are prevalent. The H9N2 strain of avian influenza virus (AIV) and Escherichia coli (E. coli) are common poultry pathogens that limit the development of the poultry industry. This study aimed to clarify the interaction between these two pathogens and their pathogenic mechanism using a mouse model. Co-infection with H9N2 AIV and E. coli significantly increased the mortality rate of mice compared to single viral or bacterial infections. It also led to the development of more severe lung lesions compared to single viral or bacterial infections. Co-infection further causes a storm of cytokines, which aggravates the host’s disease by regulating the STAT/SOCS and ERK1/2 pathways. Moreover, co-infection mutually benefited the virus and the bacteria by increasing their multiplication rates. Importantly, nitric oxide synthase 2 (NOS2) expression was also significantly enhanced by the co-infection. It played a key role in the rapid proliferation of E. coli in the presence of the coinfecting H9N2 virus. Therefore, our study underscores the role of NOS2 as a determinant for bacteria growth and illustrates its importance as an additional mechanism that enhances influenza virus-bacteria synergy. It further provides a scientific basis for investigating the synergistic infection mechanism between viruses and bacteria.
2021-04-08 | GSE164963 | GEO
Project description:To determine the host response to AIV in chicken lungs, a whole chicken genome array was used to analyze RNA isolated from chicken lungs infected with AIV (4dpi) or medium control (NS). Dual-color, direct comparisons were carried between AIV infected and non-infected controls. Each comparison includes four biological replicates. There were 508 mRNAs (347 down-regulated) were differentially expressed following AIV infection. From the results, MX1, IL-8, IRF-7, TNFRS19 are identified as strong candidate genes involved in regulating the host response to AIV infection in the lungs of broiler chickens. Further gene specific knock-down assay is warranted to elucidate underlying mechanism of AIV infection regulation in the chicken. Dual-color, common reference comparisons were carried between AIV infected and non-infected controls. Four biological replicates, with dye swap labeling, were included in the comparisons. Background subtracted signal intensity were collected from 4 arrays and normalized before data analysis.
2012-06-06 | E-GEOD-38197 | biostudies-arrayexpress
Project description:Wild bird virus isolates of various subtypes from the Netherlands
| PRJNA322646 | ENA
Project description:Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes. AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.
2025-07-28 | GSE296526 | GEO
Project description:Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes (DE300 and DE256 were AT and DE558 and DE213 were not AT). AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.
2025-07-28 | GSE298058 | GEO
Project description:To determine the host response to AIV in chicken lungs, a whole chicken genome array was used to analyze RNA isolated from chicken lungs infected with AIV (4dpi) or medium control (NS). Dual-color, direct comparisons were carried between AIV infected and non-infected controls. Each comparison includes four biological replicates. There were 508 mRNAs (347 down-regulated) were differentially expressed following AIV infection. From the results, MX1, IL-8, IRF-7, TNFRS19 are identified as strong candidate genes involved in regulating the host response to AIV infection in the lungs of broiler chickens. Further gene specific knock-down assay is warranted to elucidate underlying mechanism of AIV infection regulation in the chicken.
2012-06-07 | GSE38197 | GEO