Influenza A virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA298520 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CDC Genomic Antiviral Surveillance - Influenza H1
| PRJNA1338246 | ENA
Project description:CDC Genomic Antiviral Surveillance - Influenza H3
| PRJNA1338247 | ENA
Project description:CDC Genomic Antiviral Surveillance - Influenza B-vic
| PRJNA1338249 | ENA
Project description:Small RNAs were profiled during influenza A virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response.
2013-09-15 | GSE48036 | GEO
Project description:Multidisciplinary studies investigating the natural history of influenza in swine
| PRJNA292781 | ENA
Project description:RNA interference (RNAi) is a key antiviral immune mechanism in eukaryotes. However, in vertebrates such as birds and mammals, antiviral RNAi has only been observed in cells with poor interferon systems (stem cells and oocytes) or in viral suppressors of RNAi (VSR) deficiency virus infections. Our research originally discovered that infecting macrophages with wild-type coronavirus (Infectious bronchitis virus, IBV) and influenza viruses (Avian influenza virus, AIV) can trigger RNAi antiviral immunity and produce a certain amount of virus-derived siRNA (vsiRNA). These vsiRNAs have an inhibitory effect on the virus and carry out targeted silencing along the Dicer-Ago2-vsiRNA axis. Notably, these vsiRNAs are distributed throughout of the virus’s entire genome, with a predilection for A/U at the 5’ and 3’ termini of vsiRNA. In addition, Dicer cleavage produces vsiRNA based on the RWM motif, where R represents A/G, W represents A/C, and M represents A/U. Additionally, we discovered that avian LGP2 and MDA5 proteins positively impact the expression of the Dicer protein and the Dicer subtype “DicerM”, which exhibits a potent antiviral activity compared to Dicer itself. Most importantly, the psilencer4.1-plasmid constructed based on vsiRNA combined with nanomaterial polyetherimide (PEI) showed excellent anti-virus activity in specific-pathogen-free (SPF) chickens. These findings show that RNA viruses trigger the production of the vsiRNA in avian somatic cells, which is of great significance for the application of therapeutic vaccines in poultry.
2025-02-26 | GSE285056 | GEO
Project description:RNA interference (RNAi) is a key antiviral immune mechanism in eukaryotes. However, in vertebrates such as birds and mammals, antiviral RNAi has only been observed in cells with poor interferon systems (stem cells and oocytes) or in viral suppressors of RNAi (VSR) deficiency virus infections. Our research originally discovered that infecting macrophages with wild-type coronavirus (Infectious bronchitis virus, IBV) and influenza viruses (Avian influenza virus, AIV) can trigger RNAi antiviral immunity and produce a certain amount of virus-derived siRNA (vsiRNA). These vsiRNAs have an inhibitory effect on the virus and carry out targeted silencing along the Dicer-Ago2-vsiRNA axis. Notably, these vsiRNAs are distributed throughout of the virus’s entire genome, with a predilection for A/U at the 5’ and 3’ termini of vsiRNA. In addition, Dicer cleavage produces vsiRNA based on the RWM motif, where R represents A/G, W represents A/C, and M represents A/U. Additionally, we discovered that avian LGP2 and MDA5 proteins positively impact the expression of the Dicer protein and the Dicer subtype “DicerM”, which exhibits a potent antiviral activity compared to Dicer itself. Most importantly, the psilencer4.1-plasmid constructed based on vsiRNA combined with nanomaterial polyetherimide (PEI) showed excellent anti-virus activity in specific-pathogen-free (SPF) chickens. These findings show that RNA viruses trigger the production of the vsiRNA in avian somatic cells, which is of great significance for the application of therapeutic vaccines in poultry.
2025-02-26 | GSE285054 | GEO
Project description:Influenza A virus (IAV) is the etiological agent of a highly contagious acute respiratory disease, which causes a considerable socioeconomic burden despite annual vaccination campaigns. Therefore, it is essential to better understand IAV-host cells interaction to help design innovative antiviral therapies. In that regard, recent studies revealed the interplay between metabolic and immune signaling pathways. However, it remains unknown whether IAV alters lung tissues metabolism and what is its potential functional consequence. Using in vitro and in vivo models as well as human respiratory fluids and in-depth metabolomics analysis, we first found that IAV infection alters the glycolysis and mitochondrial oxidative respiration in lung tissues, leading to the accumulation of several immunometabolites in the bronchoalveolar airspaces. We next focused on one mitochondria-derived metabolite, i.e. succinate as its accumulation was found not only in the lungs of IAV-challenged mice but also in the tracheal fluids of IAV-infected patients. Remarkably, we found that succinate exhibits a potent antiviral activity both in vitro and in vivo as it inhibits H1N1 and H3N2 IAV strains and it strongly decreases IAV-triggered inflammatory response. The underlying inhibiting mechanism involves a disruption of IAV replication cycle. Indeed, succinate prevents specifically the nuclear export of the viral nucleoprotein NP, likely due to a specific succinylation at K87 site. Finally, we showed that mice receiving succinate through the intranasal route are more resistant to IAV pneumonia than mock-treated animals. Hence, our study identifies the metabolite succinate as a novel component of the host antiviral arsenal.
2022-03-24 | PXD018419 | Pride
Project description:The 1918 influenza pandemic was unusually severe, resulting in about 50 million deaths worldwide. A reconstructed version of the 1918 (H1N1) virus has been shown to also highly pathogenic in mice; however, the potential virulence and pathogenicity of the 1918 virus in nonhuman primates in unknown. In these studies, we demonstrate that the 1918 virus caused a highly pathogenic respiratory infection in a cynomolgus macaque model that culminated in acute respiratory distress and a fatal outcome. To characterize the global gene expression host response, oligonulceotide microarray analysis was performed on RNA isolated from the bronchus of macaques infected with either the 1918 virus or a humanized contemporary H1N1 influenza virus (A/Kawasaki/173/01). These experiments showed that infected animals mounted an immune response, characterized by dysregulation of the antiviral response, that was insufficient for protection, suggesting that atypical host innate immune responses may contribute to lethality.
2007-01-18 | E-TABM-181 | biostudies-arrayexpress
Project description:Metabolic pathways instructing the cellular fate and function, however, the exact roles of metabolites in host immune responses remain undefined. Using unbiased metabolomics and pharmacological inhibition analysis, we report natural metabolic intermediate, oxaloacetate (OAA) primes effective broad-spectrum innate immunity against viral infection. OAA serves as an immune signal, rather than alters the metabolic flux to prompt antiviral immunity. Malate dehydrogenase 1 (MDH1) senses OAA to undergo dimerization, thus functions as a scaffold to recruit transcription factor ETS2 for phosphorylation by kinase TAOK1 at serine 313. Phosphorylated ETS2 is involved in the transcriptional regulation of TANK-binding kinase 1 (TBK1). OAA deficiency caused by genetic ablation and enzymatic inhibition of the ATP-citrate lyase (ACLY) decreases the antiviral immune responses through MDH1-TAOK1-ETS2-TBK1 pathway in vivo, and makes mice more susceptible to lethal viral infection. Taken together, our findings delineate an OAA-initiated immunometabolic circuit that links metabolic pathway and antiviral immune responses.
2025-07-19 | GSE259217 | GEO