Avian coronavirus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA267235 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1664403.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:Avian coronavirus Genome sequencing and assembly
| PRJNA912654 | ENA
Project description:Avian coronavirus strain:Beaudette Genome sequencing and assembly
| PRJNA736341 | ENA
Project description:Background：Dendritic cells (DCs), have the most important antigen presenting ability and played an irreplaceable role in recognizing and clearing virus. Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. MicroRNA, small non-coding RNAs, that can regulate dendritic cells to inhibit the infection and replication of avian influenza virus. Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. Results： Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. First, we found that both active and inactive H9N2 AIV enhance the ability of DCs to present antigens and activate T lymphocytes. Next, total microarray analyses suggested that H9N2 AIV stimulation involved in protein localization, nucleotide binding and leukocyte transendothelial migration and MAPK signal pathways. Moreover, we construct 551 transcription factor (TF)-microRNA-mRNA loops based on the above analyses. Furthermore, we found that HA fragment could not activate DCs, while truncated HA highly increased the immune function of DCs by activating ERK and STAT3 signal pathway. Last, our insight research not only gained that gga-miR1644 might target to MBNL2 to enhanced avian DCs in inhibiting virus replication, but also suggested that gga-miR6675 target to the NLS of PB1 to trigger the silencing of PB1 genes and lead to inhibition of H9N2 avian influenza viral replication. All together, our innovative research will shed new light on the roles of avian microRNA in evoking avian DCs and inhibiting virus replication, which will suggest new strategies to combat avian influenza virus.
2017-07-08 | GSE100916 | 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 | 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: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 | GSE285055 | GEO
Project description:A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV.
2014-01-16 | GSE49840 | GEO
Project description:A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV. Here, polarized confluent monolayers of Calu-3 cells were infected apically with the avian-origin IAVs A/Anhui/01/2013 (H7N9) [Anhui01], A/Netherland/219/2003 (H7N7) [NL219], A/Vietnam/1203/2004 (H5N1) [VN1203], or a human seasonal virus A/Panama/2007/1999 (H3N2) [Pan99] at an MOI of 1. Time-matched mocks were also included using the same cell stock as the rest of the samples. Culture medium (same as what the virus stock is in) was used for the mock infections. Quadruplicate wells were infected for each virus/timepoint. Measured timepoints were 3, 7, 12 and 24 hours post-inoculation and the RNA was used for transcriptional analysis via microarray.
2014-01-16 | E-GEOD-49840 | biostudies-arrayexpress