Ontology highlight
ABSTRACT:
PROVIDER: PRJNA787639 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR17290200_1.fastq.gz | Fastqsanger.gz | |||
| SRR17290200_2.fastq.gz | Fastqsanger.gz | |||
| SRR17290201_1.fastq.gz | Fastqsanger.gz | |||
| SRR17290201_2.fastq.gz | Fastqsanger.gz |
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Project description:Airway epithelial cells are the initial site of infection with influenza viruses. The innate immune responses of airway epithelial cells to infection have the potential to limit virus replication and induce effective adaptive immune responses. However, relatively little is known about the importance of this innate anti-viral response to infection. Avian influenza viruses are a potential source of future pandemics, therefore it is critical to examine the effectiveness of the host anti-viral system to different influenza viruses. We used a human influenza (H3N2) and a low pathogenic avian influenza (H11N9) to assess and compare the anti-viral responses of bronchial epithelial cells (BECs). After infection, the H3N2 virus replicated more effectively than the H11N9 strain in BECs. This was not due to differential expression of different sialic acid residues on BECs but was attributed to the interference of the host anti-viral responses by H3N2. The H3N2 strain induced a delay in anti-viral signaling and impaired release of type I and type III interferons (IFNs) compared to the H11N9 virus. We then transfected the gene encoding for non-structural (NS) 1 protein into the BECs and the H3N2 NS1 induced a greater inhibition of anti-viral responses compared to the H11N9 NS1. While the low pathogenic avian influenza virus was capable of infecting BECs, the human influenza virus replicated more effectively than avian influenza virus in BECs and this may be at least in part due to a differential ability of the two NS1 proteins to inhibit anti-viral responses. This suggests that the subversion of human anti-viral responses may be an important requirement for influenza viruses to adapt to the human host and induce disease.
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Project description:Virus infection induces activation and suppression of global gene expression in the host. Profiling gene expression changes in the host may provide insights into the molecular mechanisms that underlie host physiological and phenotypic responses to virus infection. In this study, the Arabidopsis Affymetrix ATH1 whole genome array was used to assess global gene expression changes in Arabidopsis thaliana plants infected with Plum pox virus (PPV). To identify early genes in response to PPV infection, an Arabidopsis synchronized single-cell transformation system was developed. Arabidopsis protoplasts were transfected with a PPV infectious clone, PPV-SK68 and global gene expression changes in the transfected protoplasts were profiled. Keywords: Time course and cell type comparison
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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.
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