Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786297 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17134346.fastq.gz | Fastqsanger.gz | |||
| SRR17134346_1.fastq.gz | Fastqsanger.gz | |||
| SRR17134346_2.fastq.gz | Fastqsanger.gz | |||
| SRR17134347.fastq.gz | Fastqsanger.gz | |||
| SRR17134347_1.fastq.gz | Fastqsanger.gz |
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Project description:Influenza A virus (IAV), one of the most prevalent respiratory diseases, causes pandemics around the world. The multifunctional non-structural protein 1 (NS1) of IAV is a viral antagonist that suppresses host antiviral response. However, the mechanism by which NS1 modulates the RNA interference (RNAi) pathway remains unclear. Here, we identified interactions between NS1 proteins of Influenza A/PR8/34 (H1N1; IAV-PR8) and Influenza A/WSN/1/33 (H1N1; IAV-WSN) and Dicer’s cofactor TAR-RNA binding protein (TRBP). We found that the N-terminal RNA binding domain (RBD) of NS1 and the first two domains of TRBP protein mediated this interaction. Furthermore, two amino acid residues (Arg at position 38 and Lys at position 41) in NS1 were essential for the interaction. We generated TRBP knockout cells and found that NS1 instead of NS1 mutants (two-point mutations within NS1, R38A/K41A) inhibited the process of microRNA (miRNA) maturation by binding with TRBP. PR8-infected cells showed masking of short hairpin RNA (shRNA)-mediated RNAi, which was not observed after mutant virus-containing NS1 mutation (R38A/K41A, termed PR8/3841) infection. Moreover, abundant viral small interfering RNAs (vsiRNAs) were detected in vitro and in vivo upon PR8/3841 infection. We identify, for the first time, the interaction between NS1 and TRBP that affects host RNAi machinery.
2022-04-15 | GSE189776 | GEO
Project description:To identify the dysregulated circRNAs expression during IAV infection, A549 cells were inoculated with PR8 (MOI = 2) and harvested at 24 h p.i., while uninfected samples were regarded as controls. Subsequently the high-throughput circRNA microarray was performed (Arraystar Human circRNA Array V2).
2025-01-28 | GSE197125 | GEO
Project description:Background: The role of host encoded microRNAs in genetically determined host susceptibility to influenza A virus (IAV) infection has not been explored. We therefore compared changes in pulmonary miRNA expression during IAV infection in two inbred mouse strains with differential susceptibility to IAV infection. Results: miRNA expression profiles were determined in lungs of the more susceptible mouse strain DBA/2J and the less susceptible strain C57BL/6J within 120 hours post infection (hpi) with IAV (H1N1) PR8. Even the miRNomes of uninfected lungs differed substantially between the two strains. After a period of relative quiescence, major miRNome reprogramming was detected in both strains by 48 hpi and increased through 120 hpi. Distinct groups of miRNAs regulated by IAV infection could be defined: (1) miRNAs (n= 39) whose expression correlated with HA mRNA expression and represented the general response to IAV infection independent of host genetic background; (2) miRNAs (n=20) whose expression correlated with HA mRNA expression but differed between the two strains; and (3) remarkably, miRNAs (n=8) whose abundance even in uninfected lungs differentiated nearly perfectly (area under the ROC curve >0.99) between the two strains throughout the time course. Higher abundance of miRNAs with anti-apoptotic functions and lower abundance of miRNAs regulating the PI3K-Akt pathway were associated with the more susceptible DBA/2J strain. Conclusions: These results suggest that differences in host miRNA abundance before and during IAV infection are in part determined genetically and contribute to susceptibility to IAV infection in this experimental mouse model, and likely in humans.
2017-06-12 | GSE89064 | GEO
Project description:Airway cell fates are altered during repair and regeneration following lung injury. Here we survey mouse airway epithelium using single nucleus RNA-sequencing after influenza (PR8) infection and uncovered the emergence of Microfold (M) cells in the post-IAV intrapulmonary lung. These pulmonary M cells share expression signatures with the better-characterized intestinal M cells. Furthermore, similar to intestinal M cells that function by overlying lymphoid follicles in Peyer’s Patches, the post-IAV pulmonary M cells are enriched over bronchus associated lymphoid tissue (BALT), suggestive an interactive relationship.
2024-01-11 | GSE244279 | GEO
Project description:Viral infections affecting the upper or lower respiratory tract induce mucin production in the epithelial surfaces of the respiratory cells. However, a little is known about how mucins are produced on the surfaces of respiratory epithelial cells and affects viral replication. In the course of the investigation of the cellular responses in the early stage of Influenza A virus (IAV) infection, we found that two miRNAs, miR-221 and miR-17-3p, which target the mRNA of GalNAc transferase 3 (GALNT3), are rapidly down-regulated as early as 1.5 h post-infection. To understand the early host cell responses to the IAV infection, we performed miRNA microarray analysis using a human alveolar adenocarcinoma cell line, A549 cells, infected with influenza A/Puerto Rico/8/34 H1N1 (PR8) virus. We isolated the cellular RNAs at 0.5, 1.5 and 4.5 h post-infection and detected significant changes in the global profile of miRNA expression after infection with IAV. mouse embryonic fibroblasts. Each sample was run in duplicate.
2015-12-08 | E-GEOD-57508 | biostudies-arrayexpress
Project description:Our study's objective was to determine circRNA expression alterations following in vivo influenza virus infection. We challenged C57BL/6 for 48 hours with IAV-PR8. Lung samples were obtained, RNA-Seq was utilized, and the circRNAs transcriptome data was compared to the control.
2023-02-17 | GSE210688 | GEO
Project description:Transcriptome analysis of mock or H1N1 IAV PR8 infected p53WT A549 and p53null A549-KO3 cells by Affymetrix GeneChip Human Transcriptome 2.0 Arrays to achieve a set of genes those are regulated by p53 and responsive to IAV infection. Influenza A virus infection activates cellular p53, however it has not been clear whether this process has pro- or anti- viral effects. In this study, using human isogenic p53 wildtype A549 cells and p53null A549-KO3 cells generated from the CRISPR/Cas9 technology, we report that p53null cells exhibit significantly reduced viral propagation property when infected with influenza A virus (H1N1/A/Puerto Rico/8/34). Here, using genome-wide microarray analysis we revealed that p53 regulates the expression of a large set of interferon-inducible genes, some of which are directly associated with viral infectivity and later experimentally validated to be responsible for p53-regulated IAV infectivity.
2018-05-31 | GSE106279 | GEO
Project description:The airway epithelium, consisting of diverse cell types, plays a vital role in defending against respiratory viruses. MIWI2 multiciliated (M2MC) cells are a rare subpopulation of multiciliated cells distinguished by the expression of MIWI2, the mouse analogous PIWIL4 argonaute family protein. While recognized for its role in repressing retrotransposons during spermatogenesis and regulating viral RNA in mosquitos, the function of MIWI2 in M2MC cells remains poorly understood. This study explores the transcriptomic changes in retrotransposons, viral RNAs, and host genes in an effort to elucidate MIWI2’s role in the airway. M2MC and nonM2MC cells were sorted from digested lungs of MIWI2 haplosufficient (Miwi2+/tom) and deficient (Miwi2tom/tom) mice intratracheally instilled with saline or mouse adapted A/Puerto Rico/8/1934 (PR8) IAV three days post infection. Our findings indicated that retrotransposon and viral RNA expression is independent of MIWI2 expression. However, MIWI2 deficiency decreased mitochondrial and ribosomal gene expression in M2MC cells during PR8 infection. In addition, a decrease in small RNAs mapped to nuclear mitochondrial (NuMT) DNA was observed in saline treated MIWI2 expressing cells. These findings were then followed up by flow cytometry studies where an increase in intracellular reactive oxygen species (ROS) was observed in PR8 infected multiciliated cells from Miwi2tom/tom mice. In addition, Miwi2tom/tom mice experience decreased viral titer and RNA 7 days post infection and recovered faster in percent body weight compared to wild-type and Miwi2+/tom mice. These studies suggest that MIWI2 exacerbates IAV outcomes by regulating mitochondrial gene expression and function. These results reveal a novel role for MIWI2 in somatic cells and propose MIWI2/PIWIL4 as a potential biomarker for susceptibility to severe respiratory infections. Understanding MIWI2-dependent pathways could lead to new therapeutic targets for respiratory viral infections.
2025-02-25 | GSE276578 | GEO
Project description:Transcriptome profiling of lung tissues and lung CD8+ TRM during early phase of infection to investigate the mechanism of lung TRM cells during antigen re-exposure within 48hours. After P14 T cell transfer, PR8 infection would not induce P14 TRM cells, while PR8-gp33 would. Comparing the gene expression of lung tissues after LCMV Armstrong challenge at day 30 after PR8 or PR8-gp33 infection would help us understand the function of lung CD8+ TRM cells. Sorted TRM cells from mice challenged with LCMV Armstrong at day 30 after PR8-gp33 infection would reveal the activation mechanism of TRM cells.
2023-10-01 | GSE186762 | GEO
Project description:Alternative polyadenylation (APA) leading to changes of mRNA 3’UTRs has been associated to numerous pathologies but its molecular origin and functional consequences often remain enigmatic. We show that all Influenza A virus (IAV) strains cause APA of host transcripts and mapped the effect to a drug-targetable glycine residue (G184) in the viral non-structural protein 1 (NS1) that is required for its interaction with CPSF4. Unexpectedly, this interaction is also conserved in IAVs not causing virus-induced transcriptional shutoff and introduction of G184R in NS1 alleviates APA. Functionally, a recombinant PR8 (NS1-G184R) virus elicited increased secretion of inflammatory cytokines as compared to the parental wild-type in vitro and in vivo, and had a strongly attenuated phenotype in vivo. Finally, we show that many pathogens induce APA, which is potentially used towards similar immunomodulatory effects.
2023-07-12 | PXD040456 | Pride