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Identification of common genes of rhinovirus single/double‑stranded RNA‑induced asthma deterioration by
1Department of Respiratory and Critical Care Medicine, Wuhu Hospital of Traditional Chinese Medicine, Wuhu, Anhui 241000, P.R. China.
Abstract:
Rhinovirus (RV) is the most common respiratory virus affecting humans. The majority of asthma deteriorations are triggered by RV infections. However, whether the effects of RV single- and double-stranded RNA on asthma deterioration have common target genes needs to be further studied. In the present study, two datasets (GSE51392 and GSE30326) were used to screen for common differentially expressed genes (cDEGs). The molecular function, signaling pathways, interaction networks, hub genes, key modules and regulatory molecules of cDEGs were systematically analyzed using online tools such as Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, STRING and NetworkAnalyst. Finally, the hub genes STAT1 and IFIH1 were verified in clinical samples using reverse transcription-quantitative PCR (RT-qPCR). A total of 85 cDEGs were identified. Function analysis revealed that cDEGs served an important role in the innate immune response to viruses and its regulation. Signal transducer and activator of transcription 1 (STAT1), interferon induced with helicase C domain 1 (IFIH1), interferon regulatory factor 7 (IRF7), DExD/H box helicase 58 (DDX58) and interferon-stimulating gene 15 (ISG15) were detected to be hub genes based on the protein-protein interactions and six topological algorithms. A key module involved in influenza A, the Toll-like receptor signaling pathway, was identified using Cytoscape software. The hub genes were regulated by GATA-binding factor 2 and microRNA-146a-5p. In addition, RT-qPCR indicated that the expression levels of the hub genes STAT1 and IFIH1 were low during asthma deterioration compared with post-treatment recovery samples. The present study enhanced the understanding of the mechanism of RV-induced asthma deterioration.
Insights
Rhinovirus infections worsen asthma by affecting common genes involved in the innate immune response. Key genes STAT1 and IFIH1 show reduced expression during asthma attacks, highlighting their role in rhinovirus-induced asthma deterioration.
Area of Science:
- Immunology
- Genomics
- Respiratory Medicine
Background:
- Rhinovirus (RV) is a primary cause of respiratory infections and a major trigger for asthma exacerbations.
- The specific genetic mechanisms linking RV infection to asthma deterioration require further investigation, particularly concerning common target genes of RV RNA.
Purpose of the Study:
- To identify common differentially expressed genes (cDEGs) affected by RV infection in asthma.
- To elucidate the molecular functions, pathways, and regulatory networks of these cDEGs.
- To validate key genes involved in RV-induced asthma deterioration.
Main Methods:
- Analysis of two public gene expression datasets (GSE51392 and GSE30326) to identify cDEGs.
- Bioinformatic analyses including Gene Ontology, KEGG pathway analysis, protein-protein interaction networks (STRING, NetworkAnalyst), and module identification (Cytoscape).
- Validation of hub genes (STAT1, IFIH1) using reverse transcription-quantitative PCR (RT-qPCR) in clinical samples.
Main Results:
- Identified 85 common differentially expressed genes (cDEGs) primarily involved in innate immune responses to viral infections.
- Discovered key hub genes including Signal transducer and activator of transcription 1 (STAT1) and Interferon induced with helicase C domain 1 (IFIH1).
- Confirmed a significant downregulation of STAT1 and IFIH1 expression during asthma deterioration compared to recovery phases.
Conclusions:
- RV infection impacts asthma deterioration through common target genes regulating innate immunity.
- STAT1 and IFIH1 are critical hub genes in the pathogenesis of RV-induced asthma exacerbations.
- Reduced expression of STAT1 and IFIH1 during deterioration suggests their protective role and potential as therapeutic targets.
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