Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13501042_1.fastq.gz | Fastqsanger.gz | |||
| SRR13501042_2.fastq.gz | Fastqsanger.gz | |||
| SRR13501043_1.fastq.gz | Fastqsanger.gz | |||
| SRR13501043_2.fastq.gz | Fastqsanger.gz | |||
| SRR13501044_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Acute viral bronchiolitis (NMS)
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Project description:Acute viral bronchiolitis (PBMC)
| PRJNA450430 | ENA
Project description:Human respiratory syncytial virus (HRSV) is the main cause of bronchiolitis during the first year of life, but other viruses such as rhinovirus also occur and are clinically indistinguishable. In hospitalized infants with bronchiolitis, the analysis of the peripheral blood mononuclear cells (PBMC) gene expression might be useful for identification the etiologies caused by HRSV and human rhinovirus (HRV) and to the development of future tests, as well as to elucidate the pathogenic mechanisms triggered by different viral agents and new therapeutic possibilities. In this study, we conducted a comparative global gene expression analysis of infants with acute viral bronchiolitis infected by HRSV (HRSV group) or HRV (HRV group).
2019-03-19 | GSE124124 | GEO
Project description:Respiratory Syncytial virus (RSV) is the most common cause of childhood viral bronchiolitis and lung injury. Inflammatory responses significantly contribute to lung pathologies during RSV infections and bronchiolitis but the exact mechanisms have not been completely defined. The double-stranded RNA-activated protein kinase (PKR) functions to inhibit viral replication and participates in several signaling pathways associated with innate inflammatory immune responses. Using a functionally defective PKR (PKR-/-) mouse model, we investigated the role of this kinase in early events of RSV-induced inflammation. Our data showed that bronchoalveolar lavage (BAL) fluid of infected PKR-/- mice had significantly lower levels of several innate inflammatory cytokines and chemokines. Histological examinations revealed that there was less lung injury in infected PKR-/- mice as compared to the wild type. A genome-wide analysis showed that several early anti viral and immune regulatory genes were affected by PKR activation. These data suggest that PKR is a signaling molecule for immune responses during RSV infections.
2009-09-23 | GSE18170 | GEO
Project description:Temporal Transcriptomic Signatures Associated with Post-viral Bronchiolitis Sequelae in Rats
| PRJNA222273 | ENA
Project description:Background: There is limited data on how different RSV genotypes and associated viral loads influence disease phenotypes. We characterized the genetic variability of RSV strains during five non-consecutive respiratory seasons, and evaluated the role of RSV subtypes, genotypes and viral loads on clinical disease severity. Methods: Healthy infants hospitalized with RSV bronchiolitis were prospectively enrolled and nasopharyngeal samples obtained within 24h of hospitalization for RSV load quantitation by PCR, typing and genotyping. Parameters of disease severity were assessed, and multivariate models constructed to identify virologic and clinical factors predictive of clinical outcomes. Results: From March 2004 to April 2011, we enrolled 253 patients (56.5 % males; median age 2.1 (1.1-4.0) months). RSV A infections predominated over RSV B (69% vs. 31%; p<0.001) and showed greater genotype variability. The most common genotypes were RSV A/GA2, A/GA5 and RSV B/BA. Infants infected with RSV GA5 had higher viral loads compared with GA2 or BA infection (p<0.01), independent of duration of symptoms. After adjusting for other covariates, RSV A/GA5 infections were associated with longer hospital stay. Conclusions: RSV A infections were more frequent than RSV B infections and displayed greater genetic variability. Infections with GA5 were independently associated with clinical disease severity.
2018-03-21 | GSE103842 | GEO
Project description:Paramyxoviruses are negative sense single-stranded RNA viruses that comprise many important human and animal pathogens, including human parainfluenza viruses. These viruses bud from the plasma membrane of infected cells after the viral ribonucleoprotein complex (vRNP) is transported from the cytoplasm to the cell membrane via Rab11a marked recycling endosomes. The viral proteins that are critical for mediating this important initial step in viral assembly are unknown. Here we use the model paramyxovirus, murine parainfluenza virus 1, or Sendai virus (SeV), to investigate the roles of viral proteins in Rab11a-driven virion assembly. We previously reported that infection with SeV containing high levels of copy-back defective viral genomes (DVGs) generates heterogenous populations of cells, with cells enriched in full-length virus producing viral particles containing standard or defective viral genomes, while cells enriched in DVGs did not, despite high levels of defective viral genome replication. Here we take advantage of this heterogenous cell phenotype to identify proteins that mediate interaction of vRNPs with Rab11a. We examine the role of matrix protein and nucleoprotein and determine that they are not sufficient to drive interaction of vRNPs and recycling endosomes. Then, using a combination of mass spectrometry and comparative protein abundance and localization in DVG- and FL-high cells, we identify viral polymerase complex components L and, specifically, its cofactor C proteins as interactors with Rab11a. We find that accumulation of these proteins within the cell is the defining feature that differentiates cells that proceed to viral egress from cells which remain in replication phases. Paramyxoviruses are a family of viruses that include a number of pathogens with significant burdens on human health. Particularly, human parainfluenza viruses are an important cause of pneumonia and bronchiolitis in children and do not have any vaccines or direct acting antivirals. These cytoplasmic replicating viruses bud from the plasma membrane and coopt cellular endosomal recycling pathways to traffic viral ribonucleoprotein complexes from the cytoplasm to the membrane of infected cells, yet the viral proteins required for viral engagement with the recycling endosome pathway is not known. Here we use the model paramyxovirus Sendai virus, or murine parainfluenza virus 1, to investigate the role of viral proteins in this initial step in viral assembly. We find that viral polymerase components large protein L and accessory C proteins are necessary for engagement with recycling endosomes. These findings are important in identifying viral targets for the development of antivirals.
2020-08-06 | PXD019637 | Pride
Project description:Experimental set 1: To evaluate the impact of apoptotic neutrophils on TLR4-induced inflammatory pathways in human macrophages. Experimental set 2: To compare the activation of inflammatory pathway between alveolar macrophages (AM) from idiopathic pulmonary fibrosis (IPF) patients and alveolar macrophages from respiratory bronchiolitis interstitial lung disease (RB-ILD) patients
2018-06-01 | GSE90010 | GEO
Project description:Despite being exposed to respiratory syncytial virus (RSV) infection multiple times in our lives, infants, older-adults, and immunocompromised patients are vulnerable to RSV-associated severe diseases, such as bronchiolitis and pneumonia. Respiratory viral infections are known to promote pulmonary fibrosis formation, which are often associated with a cellular remodeling process epithelial-mesenchymal transition (EMT). However, there is no information on whether RSV causes EMT in bronchial epithelial cells. Our results suggest that RSV-infection does not induce EMT in three different in vitro lung models: epithelial A549 cell line, primary normal human bronchial epithelial cells, and pseudostratified airway epithelium. Interestingly, RSV infection increased cell surface area and perimeter in the infected airway epithelium, which is distinct from the TGF-β1 driven cell elongation. Genome-wide transcriptome analysis also revealed that RSV infection is not involved in cell motility and locomotion. Thus, our results suggest that RSV infection does not induce EMT in the airway epithelium
2023-06-13 | GSE189537 | GEO