ArticleFrontiers in microbiology2023
Altered cell function and increased replication of rhinoviruses and EV-D68 in airway epithelia of asthma patients.
Article in Frontiers in microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Pharmacological activity, molecular mechanisms and therapeutic potential of erianin (Review).International journal of molecular medicine · 2026Review
- Double-Stapled Peptide Scan Yields Potent Fusion Inhibitors of Respiratory Syncytial Virus.Journal of medicinal chemistry · 2026Article
- Enterovirus respiratory infection in adults: an overlooked clinical burden emerging in the post-pandemic era.Le infezioni in medicina · 2026Article
- SARS-CoV-2 delta and omicron variants alter trophoblast cell fusion and syncytiotrophoblast dynamics: new insights into placental vulnerability.Cell death & disease · 2025Article
- Beyond respiratory syncytial virus and rhinovirus: The other viral respiratory bandits.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2025Review
- Models to evaluate the pulmonary toxicity of desert dust and what we have learned from them so far: a mini-review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- EV-D68 cleaves LARP1 and PABPC1 by 3Cpro to redirect host mRNA translation machinery toward its genomic RNA.PLoS pathogens · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Rhinovirus (RV) infections constitute one of the main triggers of asthma exacerbations and an important burden in pediatric yard. However, the mechanisms underlying this association remain poorly understood. Methods: In the present study, we compared infections of Results: We found that viral replication was higher in tissues derived from asthmatic donors for all tested viruses. Viral receptor expression was comparable in non-infected tissues from both groups. After infection, ICAM1 and LDLR were upregulated, while CDHR3 was downregulated. Overall, these variations were related to viral replication levels. The presence of the CDHR3 asthma susceptibility allele (rs6967330) was not associated with increased RV-C replication. Regarding the tissue response, a significantly higher interferon (IFN) induction was demonstrated in infected tissues derived from asthmatic donors, which excludes a defect in IFN-response. Unbiased transcriptomic comparison of asthmatic versus control tissues revealed significant modifications, such as alterations of cilia structure and motility, in both infected and non-infected tissues. These observations were supported by a reduced mucociliary clearance and increased mucus secretion in non-infected tissues from asthmatic donors. Discussion: Altogether, we demonstrated an increased permissiveness and susceptibility to RV and respiratory EV infections in HAE derived from asthmatic patients, which was associated with a global alteration in epithelial cell functions. These results unveil the mechanisms underlying the pathogenesis of asthma exacerbation and suggest interesting therapeutic targets.
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