Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA267575 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Elucidate RSV-host-microbiome determinants that influence pathogenesis and subsequent childhood asthma
| PRJNA267583 | ENA
Project description:Viral infection perturbs host cells and can be used to uncover host regulatory mechanisms controlling both cell response and homeostasis. Here, using cell biological, biochemical and genetic tools, we reveal that influenza virus infection induces global transcriptional defects at the 3’-end of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. This effect induces the biogenesis of aberrant RNAs (3’-extensions and host gene fusions) which ultimately causes global transcriptional downregulation of physiological transcripts, an effect that impacts antiviral response and virulence. We show that this phenomenon occurs with multiple strains of influenza virus and it is dependent on influenza NS1 protein expression. Mechanistically, pervasive RNAPII run-through can be modulated by SUMOylation of an intrinsically disordered region (IDR) of the NS1 expressed by the 1918 pandemic influenza virus. SUMOylation increases NS1 partitioning in nuclear granules and interference with the host transcriptional apparatus which result in augmentation of termination defects and a concomitant increase in global host gene shut off. Our data identify a general strategy used by influenza virus to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins, along with human genetic variation in enzymes that metabolize post-translational modifications, can determine the outcome of an infection. We thus propose that analysis of strain-specific determinant of pathogenesis can shed light on the molecular basis of virulence.
2018-09-05 | GSE103604 | GEO
Project description:Exposing influenza B: interrogating the evolution and changing host response to the other influenza
| PRJNA1182786 | ENA
Project description:Exposing influenza B: interrogating the evolution and changing host response to the other influenza
| PRJNA1182784 | ENA
Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison.
2013-04-17 | GSE46087 | GEO
Project description:Seasonal influenza outbreaks represent a large burden for the healthcare system as well as the economy. While the role of the microbiome in the context of various diseases has been elucidated, the effects on the respiratory and gastrointestinal microbiome during influenza illness is largely unknown. Therefore, this study aimed to characterize the temporal development of the respiratory and gastrointestinal microbiome of swine using a multi-omics approach prior and during influenza infection. Swine is a suitable animal model for influenza research, as it is closely related to humans and a natural host for influenza viruses. Our results showed that IAV infection resulted in significant changes in the abundance of Moraxellaceae and Pasteurellaceae families in the upper respiratory tract. To our surprise, temporal development of the respiratory microbiome was not affected. Furthermore, we observed significantly altered microbial richness and diversity in the gastrointestinal microbiome after IAV infection. In particular, we found increased abundances of Prevotellaceae, while Clostridiaceae and Lachnospiraceae decreased. Furthermore, metaproteomics showed that the functional composition of the microbiome, known to be robust and stable under healthy conditions, was heavily affected by the influenza infection. Metabolome analysis proved increased amounts of short-chain fatty acids in the gastrointestinal tract, which might be involved in faster recovery. Furthermore, metaproteome data suggest a possible immune response towards flagellated Clostridia induced during the infection. Therefore, it can be assumed that the respiratory infection with IAV caused a systemic effect in the porcine host and microbiome.
2022-02-16 | PXD024077 | Pride
Project description:Influenza A virus (IAV) lacks the enzyme for adding 5â caps to its RNAs, and thus snatches the 5â ends of host capped RNAs to prime transcription. Neither the preference of the host RNA sequences snatched, nor the effect of âcap-snatchingâ on host processes has been completely defined. Previous studies of influenza cap-snatching used poly(A)-selected RNA from infected cells or relied solely on annotated host protein-coding genes to define host mRNAs selected by the virus. To examine the substrate-product relationship between all host RNAs, including non-coding RNAs, and viral RNAs, we used an unbiased approach to identify the host and viral capped RNAs from IAV-infected cells. We demonstrate that IAV predominantly snatches caps from non-coding host RNAs, particularly U1 and U2 small nuclear RNAs (snRNAs). Because snRNAs regulate host mRNA processing, cap-snatching of snRNAs may constitute a means by which IAV hijacks host cell metabolism. examine caps snatched by influenza virus A
2015-11-23 | E-GEOD-67493 | biostudies-arrayexpress
Project description:Intra- and inter-host evolutionary dynamics of mammalian influenza viruses
| PRJNA255651 | ENA
Project description:Influenza A virus is a kind of single negative-stranded RNA virus which belongs to the Orthomyxoviridae family. It can cause localized outbreak or worldwide epidemic in a short time for its great contagiosity, fast spread speed and a wide range of host, and H1N1 influenza virus is a strong pathogenic subtype of influenza A virus. Influenza A virus infection has been shown to alter miRNA expression both in cultured cells and in animal models. We used microRNA microarrays to detail the programme of microRNA expression and identified distinct classes of differentially regulated microRNAs during this process.
2014-10-21 | GSE62495 | GEO
Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease. Calu-3 cells were infected with VN1203 influenza virus and profiled at 0, 3, 7, 12, 18, and 24 hours post infection. There are 3 mock and infected replicates for each time point.
2011-09-01 | E-GEOD-28166 | biostudies-arrayexpress