Bacteria/variant of Metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA451254 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7051780.fastq.gz | Fastqsanger.gz | |||
| SRR7051790.fastq.gz | Fastqsanger.gz | |||
| SRR7051800.fastq.gz | Fastqsanger.gz | |||
| SRR7051810.fastq.gz | Fastqsanger.gz | |||
| SRR7051820.fastq.gz | Fastqsanger.gz |
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Project description:Nasopharyngeal microbiota profiles Microbiome Utrecht Infant Study (MUIS) up until one year of age.
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Project description:Respiratory syncytial virus (RSV) selectively targets ciliated cells in human bronchial epithelium and can cause bronchiolitis and pneumonia mostly in infants. To identify molecular targets of intervention during RSV infection in infants, we investigate how age regulates RSV interaction with the bronchial epithelium barrier. Employing precision-cut lung slices and air-liquid interface cultures generated from infant and adult human donors, we found robust RSV virus spread and extensive apoptotic cell death only in infant bronchial epithelium. In contrast, adult bronchial epithelium showed insignificant barrier damage and limited RSV infection. Single nuclear RNA-sequencing revealed age-related insufficiency of an anti-apoptotic STAT3 activation response to RSV infection in infant ciliated cells, which was exploited to facilitate virus spread via the extruded apoptotic ciliated cells carrying RSV. Activation of STAT3 and blockade of apoptosis rendered protection against severe RSV infection in infant bronchial epithelium. Lastly, apoptotic inhibitor treatment of a neonatal mouse model of RSV infection ameliorated infection and inflammation in the lung. Taken together, our findings identify a STAT3-mediated anti-apoptosis pathway as a target to battle severe RSV disease in infants.
2024-09-30 | GSE274466 | GEO
Project description:Rationale: Respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory tract infections and hospitalizations in infants worldwide. Known risk factors, however, incompletely explain the variability of RSV disease severity among children. We postulate that severity of RSV infection is influenced in part by modulation of the host immune response by the local microbial ecosystem at the time of infection. Objectives: To define whether different nasopharyngeal microbiota profiles are associated with distinct host transcriptome profiles and severity in children with RSV infection. Methods: We analyzed the nasopharyngeal microbiota profiles of young children with mild and severe RSV disease and healthy matched controls by 16S-rRNA sequencing. In parallel, we analyzed whole blood gene expression profiles to study the relationship between microbial community composition, the RSV-induced host transcriptional response and clinical disease severity. Measurements and Main results: We identified five nasopharyngeal microbiota profiles characterized by enrichment of H. influenzae, Streptococcus, Corynebacterium, Moraxella or S. aureus. RSV infection and RSV hospitalization were positively associated with H. influenzae and Streptococcus, and negatively associated with S. aureus abundance, independent of age. The host response to RSV was defined by overexpression of interferon-related genes, and this was independent of the microbiota composition. On the other hand, transcriptome profiles of RSV infected children with H. influenzae and Streptococcus-dominated microbiota were characterized by greater overexpression of genes linked to toll-like receptor-signaling and neutrophil activation and were more frequently hospitalized Conclusions: Our data suggest an immunomodulatory role for the resident nasopharyngeal microbial community early in RSV infection, potentially affecting RSV disease severity.
2016-05-09 | GSE77087 | GEO
Project description:To study the transcriptional profile of patients with acute RSV or Influenza infection,children of median age 2.4 months (range 1.5-8.6) hospitalized with acute RSV and influenza virus infection were offered study enrollment after microbiologic confirmation of the diagnosis. Blood samples were collected from them within 42-72 hours of hospitalization. We excluded children with suspected or proven polymicrobial infections, with underlying chronic medical conditions (i.e congenital heart disease, renal insufficiency), with immunodeficiency, or those who received systemic steroids or other immunomodulatory therapies. The RSV cohort consisted of 51 patients with median age of 2 months (range 1.5-3.9) and the influenza cohort had 28 patients with median age of 5.5 months (range 1.4-21). Control samples were obtained from healthy children undergoing elective surgical procedures or at outpatient clinic visits. To exclude viral co-infections we performed nasopharyngeal viral cultures of all subjects. We recruited 10 control patients for the RSV cohort with median age of 6.7 months (range 5-10), and 12 control patients for the influenza cohort with median age of18.5 months (range 10.5-26). We used microarrays to obtain the transcriptional profile of PBMCs from patients with acute RSV or Influenza infection and compared these signatures with the transcriptional profile of primary airway epithelial cells infected with RSV or Influenza.
2012-03-12 | E-GEOD-34205 | biostudies-arrayexpress
Project description:Genome-wide analysis of transcriptional profiles in children <17 years of age with RSV infection and healthy controls
2016-05-25 | GSE80179 | GEO
Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection
2013-11-12 | GSE38900 | GEO
Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection Total RNA extracted from whole blood (lysed in Tempus tubes) drawn from individual pediatric patients with acute RSV, influenza and Rhinovirus lower respiratory tract infection. A total of 241 samples are analyzed: 135 with acute RSV LRTI, 30 with Rhinovirus LRTI, 16 with influenza LRTI, 39 age-sex matched healthy controls and 21 samples obtained one month after the acute hospitalization in children with RSV. Samples GSM1226237-GSM1226272, which were hybridized to Platform GPL10558, were normalized separately from the other Samples in this Series, which were hybridized to Platform GPL6884. 'GSE38900_non-normalized_GSM1226237-GSM1226272.txt.gz' includes the non-normalized data for Samples GSM1226237-GSM1226272; 'GSE38900_non-normalized.txt.gz' includes the non-normalized data for the other Samples.
2013-11-12 | E-GEOD-38900 | biostudies-arrayexpress
Project description:To study the transcriptional profile of patients with acute RSV or Influenza infection,children of median age 2.4 months (range 1.5-8.6) hospitalized with acute RSV and influenza virus infection were offered study enrollment after microbiologic confirmation of the diagnosis. Blood samples were collected from them within 42-72 hours of hospitalization. We excluded children with suspected or proven polymicrobial infections, with underlying chronic medical conditions (i.e congenital heart disease, renal insufficiency), with immunodeficiency, or those who received systemic steroids or other immunomodulatory therapies. The RSV cohort consisted of 51 patients with median age of 2 months (range 1.5-3.9) and the influenza cohort had 28 patients with median age of 5.5 months (range 1.4-21). Control samples were obtained from healthy children undergoing elective surgical procedures or at outpatient clinic visits. To exclude viral co-infections we performed nasopharyngeal viral cultures of all subjects. We recruited 10 control patients for the RSV cohort with median age of 6.7 months (range 5-10), and 12 control patients for the influenza cohort with median age of18.5 months (range 10.5-26).
2012-03-12 | GSE34205 | GEO
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:Respiratory syncytial virus (RSV) causes severe disease mostly in infants; however, mechanisms of age association remain elusive. Here, employing human bronchial epithelium models generated from tracheal aspirate-derived basal stem cells of neonates and adults, we investigate whether age regulates RSV-epithelium interaction to determine disease severity. We show that following RSV infection, only neonatal epithelium model exhibits cytopathy and mucus hyperplasia, and neonatal epithelium has more robust viral spread and inflammatory responses than adult epithelium. Mechanistically, RSV-infected neonatal ciliated cells display age-related impairment of STAT3 activation, rendering susceptibility to apoptosis, which facilitates viral spread. In contrast, SARS-CoV-2 infection of ciliated cells has no effect on STAT3 activation and is not affected by age. Taken together, our findings identify an age-related and RSV-specific interaction with neonatal bronchial epithelium that critically contributes to severity of infection, and STAT3 activation offers a potential strategy to battle severe RSV disease in infants.
2024-09-01 | GSE242397 | GEO