Global transcriptional changes induced by rhinovirus infection in-vitro
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28904 | GEO | 2014/04/01
SECONDARY ACCESSION(S): PRJNA140665
REPOSITORIES: GEO
Similar Datasets
Project description:Cell lines B2B and 16HBE were infected in-vitro with rhinovirus 16 and comparisons were made to mock-infected cultures and cultures exposed to UV-irradiated rhinovirus. Total RNA were extracted and assessed by whole genome expression arrays. Rhinovirus in-vitro infected cell lines harvested at different time points (T hours) in biological triplicates. Total RNA extracted directly upon harvest.
2014-04-01 | E-GEOD-28904 | biostudies-arrayexpress
Project description:Background: Respiratory viruses including rhinovirus can cause pulmonary exacerbations in cystic fibrosis (CF). Aberrant responses by the CF airway epithelium during rhinovirus infection, particularly interferon production, may underly the clinical observations. Whether CFTR modulators affect antiviral responses by CF epithelia is presently unknown. We tested the hypothesis that treatment of CF epithelial cells with Ivacaftor or ivacaftor/lumacaftor (Orkambi) would improve control of rhinovirus infection. Methods: Nineteen CF epithelial cultures (CFTR Class 2: 10 homozygous for p.Phe508del, CFTR Class 3: 9 p.Phe508del/p.Gly551Asp) were infected with rhinovirus 1B at multiplicity of infection 12 for 24 hours. Culture RNA and supernatants were harvested to assess gene and protein expression respectively. Results: RNA-seq analysis comparing rhinovirus infected cultures to control identified 796 and 629 differentially expressed genes for Class 2 and Class 3, respectively. This gene response was highly conserved when cells were treated; all infected cultures (+/- treatment) were associated with the same top three over-represented biological pathways associated with interferon signalling, and were predicted to be driven by the same interferon-pathway transcriptional regulators (IFNA, IFNL1, IFNG, IRF7, STAT1). Direct comparisons between treated and untreated infected cultures did not yield any differentially expressed genes for Class 3, and only 68 genes for Class 2, related to cell metabolic pathways. In addition, CFTR modulators did not affect viral copy number, or levels of pro-inflammatory cytokines produced post-infection. Conclusions: Though long term clinical data is not yet available, results presented here suggest CFTR modulators do not interfere with core airway epithelial responses to rhinovirus infection.
2020-09-01 | GSE139078 | GEO
Project description:Primary human bronchial epithelial cells were transfected with siRNA to knockdown IRF7 gene expression, allowed to recover, and then infected with human rhinovirus. At 24 hrs post rhinovirus infection, gene expression patterns were profiled on microarrays.
2016-01-10 | GSE70190 | GEO
Project description:Primary human bronchial epithelial cells were transfected with siRNA to knockdown IRF7 gene expression, allowed to recover, and then infected with human rhinovirus. At 24 hrs post rhinovirus infection, gene expression patterns were profiled on microarrays. The study design consisted of five donors, two transfection conditions (all-star negtaive control siRNA; IRF7-specific siRNA), and two culture conditions (medium control, rhinovirus-16).
2016-01-10 | E-GEOD-70190 | biostudies-arrayexpress
Project description:RATIONALE: Human rhinovirus infections cause colds and trigger exacerbations of lower airway diseases. OBJECTIVES: To define changes in gene expression profiles during in vivo rhinovirus infections. METHODS: Nasal epithelial scrapings were obtained before and during experimental rhinovirus infection, and gene expression was evaluated by microarray. Naturally acquired rhinovirus infections, cultured human epithelial cells, and short interfering RNA knockdown were used to further evaluate the role of viperin in rhinovirus infections. MEASUREMENTS AND MAIN RESULTS: Symptom scores and viral titers were measured in subjects inoculated with rhinovirus or sham control, and changes in gene expression were assessed 8 and 48 hours after inoculation. Real-time reverse transcription-polymerase chain reaction for viperin and rhinoviruses was used in naturally acquired infections, and viperin mRNA levels and viral titers were measured in cultured cells. Rhinovirus-induced changes in gene expression were not observed 8 hours after viral infection, but 11,887 gene transcripts were significantly altered in scrapings obtained 2 days postinoculation. Major groups of up-regulated genes included chemokines, signaling molecules, interferon-responsive genes, and antivirals. Viperin expression was further examined and also was increased in naturally acquired rhinovirus infections, as well as in cultured human epithelial cells infected with intact, but not replication-deficient, rhinovirus. Knockdown of viperin with short interfering RNA increased rhinovirus replication in infected epithelial cells. CONCLUSIONS: Rhinovirus infection significantly alters the expression of many genes associated with the immune response, including chemokines and antivirals. The data obtained provide insights into the host response to rhinovirus infection and identify potential novel targets for further evaluation.
2008-05-06 | GSE11348 | GEO
Project description:This study provides a comprehensive evaluation of changes in gene expression during rhinovirus infections in vivo. Subjects were experimentally infected with HRV-16 rhinovirus (RV16) or sham infected (control). Nasal epithelial scrapings collected and processed for microarray analysis. Only subjects exhibiting rhinovirus infection were analyzed. Experiment Overall Design: Randomized, parallel group study. A total of 31 subjects was analyzed: 15 infected and 16 controls. Nasal scapings were taken 14 days prior to infection (d14) and 8 hours (d0) and 2 days (d2) after infection. For each collection, alternating nostrils were used (e.g. -14d = left, 8hr = right, 2d=left) and subjects were randomized for collection (e.g. LRL, RLR).
2008-06-12 | E-GEOD-11348 | biostudies-arrayexpress
Project description:This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE).
2011-03-15 | GSE27973 | GEO
Project description:This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE). Cultured epithelial cells from each of 4 donors were exposed to medium alone, rhinovirus 16 (RV16) alone, CSE alone, or RV16 in the presence of CSE. After a 24 h incubation gene expression was assessed.
2011-03-15 | E-GEOD-27973 | biostudies-arrayexpress
Project description:Human rhinovirus and influenza virus infections of the upper airway lead to colds and the flu and can trigger exacerbations of lower airway diseases including asthma and chronic obstructive pulmonary disease. Despite modest advances in the diagnosis and treatment of infections by these viruses, novel diagnostic and therapeutic targets are still needed to differentiate between the cold and the flu, since the clinical course of influenza can be severe while that of rhinovirus is usually more mild. In our investigation of influenza and rhinovirus infection of human respiratory epithelial cells, we used a systems approach to identify the temporally changing patterns of host gene expression from these viruses. After infection of human bronchial epithelial cells (BEAS-2B) with rhinovirus, influenza virus or co-infection with both viruses, we studied the time-course of host gene expression changes over three days. From these data, we constructed a transcriptional regulatory network model that revealed shared and unique host responses to these viral infections such that after a lag of 4-8 hours, most cell host responses were similar for both viruses, while divergent host cell responses appeared after 24-48 hours. The similarities and differences in gene expression after epithelial infection of rhinovirus, influenza virus, or both viruses together revealed qualitative and quantitative differences in innate immune activation and regulation. These differences help explain the generally mild outcome of rhinovirus infections compared to influenza infections which can be much more severe. Human bronchial epithelial cells (BEAS-2B) were infected with rhinovirus, influenza virus or both viruses and RNAs were then profiled at 10 time points (2, 4, 6, 8, 12, 24, 26, 48, 60 and 72hrs)
2015-12-21 | E-GEOD-71766 | biostudies-arrayexpress