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Upper Airway Gene Expression in Hospitalized Children with Rhinovirus-induced Respiratory Illnesses
Insights
Rhinovirus (RV) and respiratory syncytial virus (RSV) infections in children trigger significant inflammatory responses. Rhinovirus, especially RV-C, uniquely upregulates genes linked to eosinophilic inflammation and mast cell activity.
Area of Science:
- Immunology
- Virology
- Transcriptomics
Background:
- Mechanisms of rhinovirus (RV)-induced respiratory illnesses remain unclear.
- Hospitalized children with viral respiratory infections require further molecular investigation.
Purpose of the Study:
- To investigate nasal transcriptomic differences in children hospitalized with RV and RSV infections.
- To elucidate virus-specific inflammatory pathways triggered by RV and RSV.
Main Methods:
- Nasal swabs collected from 46 children with RV (RV-A, RV-C), 12 with RSV, and 6 controls.
- Viral detection, genotyping, and quantification via PCR.
- Next-generation sequencing for RNA transcript analysis and differential gene expression using DESeq2.
Main Results:
- All viruses upregulated genes involved in granulocyte chemotaxis, epithelial remodeling, and antiviral responses; cilium-related genes were downregulated.
- RV induced greater expression of genes related to eosinophilic inflammation and mucus secretion compared to RSV.
- RV-C infections specifically increased mast cells and interferon-lambda (IFN-λ) mRNA expression, correlating with viral load.
Conclusions:
- Hospitalized children with RV and RSV infections exhibit distinct, robust inflammatory profiles.
- Nasal transcriptomics reveals virus-specific immune responses, offering insights into RV-C's role in respiratory illness severity.
Background:
The precise mechanisms underlying rhinovirus (RV)-induced respiratory illnesses are not completely known.
Objective:
We sought to obtain nasal transcriptomic data from hospitalized children with respiratory viral infections.
Methods:
We obtained nasal swabs from 46 children with RV (16 RV-A, 30 RV-C). For comparison, we examined swabs from 12 children with RSV and six controls. Subjects ranged in age from 1 month to 18 years. Viral detection, genotyping and copy number were determined by PCR. RNA transcripts were measured by next generation sequencing and differences in gene expression calculated using DESeq2.
Results:
Compared to controls, 1232 transcripts were upregulated (adjusted p<0.05, fold change >1.5) by all three viruses, including genes regulating granulocyte chemotaxis, cysteinyl leukotriene production, epithelial remodeling and antiviral responses. Cilium-related genes were downregulated. Compared to RSV, RV induced greater expression of 207 genes including those regulating eosinophilic inflammation, mucus secretion and mast cell function.RSV induced greater upregulation of 674 genes including those regulating neutrophilic inflammation and type 1 IFN response. Computational deconvolution of RNA-seq profiles revealed that viral infection decreased ciliated cells while increasing neutrophils, natural killer cells, monocytes (all viral species) and goblet cells (RV only). RV-C infections increased mast cells and IFN-λ mRNA expression. RV copy number correlated with the expression of mast cell proteases and numerous pro-inflammatory and IFN-stimulated genes.
Conclusion:
Children hospitalized with RV and RSV infections mount robust inflammatory responses, but virus-specific differences exist.
Clinical Implication:
These data provide insight into mechanisms by which RV, and in particular, RV-C, trigger respiratory illnesses.
Capsule Summary:
Nasal transcriptomics demonstrate that RV infections in hospitalized children induce expression of genes regulating eosinophilic inflammation, mucus secretion and mast cell function, with RV-C in particular increasing IFN-λ expression.
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