The host response to influenza virus infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA433575 | ENA |
REPOSITORIES: ENA
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2011-09-01 | E-GEOD-28166 | biostudies-arrayexpress
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2019-12-10 | GSE118773 | 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.
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Project description:While a common symptom of influenza and coronavirus disease 2019 (COVID-19) is fever, its physiological role on host resistance to viral infection remains less clear. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C increase host resistance to viral pathogens including influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). High heat-exposed mice increase basal body temperature over 38 °C to enable more bile acids production in a gut microbiota-dependent manner. The gut microbiota-derived deoxycholic acid (DCA) and its plasma membrane-bound receptor Takeda G-protein-coupled receptor 5 (TGR5) signaling increase host resistance to influenza virus infection by suppressing virus replication and neutrophil-dependent tissue damage. Furthermore, the DCA and its nuclear farnesoid X receptor (FXR) agonist protect Syrian hamster from lethal SARS-CoV-2 infection. Moreover, we demonstrate that certain bile acids are reduced in the plasma of COVID-19 patients who developed moderate I/II disease compared with minor illness group. These findings uncover an unexpected mechanism by which virus-induced high fever increases host resistance to influenza virus and SARS-CoV-2 in a gut microbiota-dependent manner.
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2011-04-27 | GSE28871 | GEO
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.
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2013-11-16 | GSE52428 | GEO
Project description:We used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1)) The Influenza A virus (A/Singapore/478/2009 (pH1N1)) infected A549 cells were harvested at 2, 4, 6, 8 and 10 hpi and RNA extraction was performed using standard protocol as described by Affymetrix. The aim of this experiment is to analyze host response to Influenza A virus (A/Singapore/478/2009 (pH1N1)) infection.
2013-01-03 | E-GEOD-31518 | biostudies-arrayexpress
Project description:As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore these, a time-course gene expression profiling was performed to detect comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs. At the age of day 35, 15 pigs were randomly allocated to the non-infected group and 15 to the infected group. Each piglet of the infected group was intranasaly challenged with A/swine/Hubei/101/2009(H1N1) strain and Each piglet of the non-infected group was treated similarly with an identical volume of PBS as control.
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