ArticleMedical microbiology and immunology2020
Differential interferon gene expression in bronchiolitis caused by respiratory syncytial virus-A genotype ON1.
Article in Medical microbiology and immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Kinetics and characterization of extracellular vesicle release from cells infected with a clinical isolate of respiratory syncytial virus A (ON1 genotype).Medical microbiology and immunology · 2026Article
- Differences Between RSV A and RSV B Subgroups and Implications for Pharmaceutical Preventive Measures.Infectious diseases and therapy · 2024Review
- NRF2 Antioxidant Response and Interferon-Stimulated Genes Are Differentially Expressed in Respiratory-Syncytial-Virus- and Rhinovirus-Infected Hospitalized Children.Pathogens (Basel, Switzerland) · 2023Article
- Expressions of Type I and III Interferons, Endogenous Retroviruses, TRIM28, and SETDB1 in Children with Respiratory Syncytial Virus Bronchiolitis.Current issues in molecular biology · 2023Article
- Proposal for Human Respiratory Syncytial Virus Nomenclature below the Species Level.Emerging infectious diseases · 2021Article
- Differential induction of type I and III interferon genes in the upper respiratory tract of patients with coronavirus disease 2019 (COVID-19).Virus research · 2021Article
- ACE2 expression is related to the interferon response in airway epithelial cells but is that functional for SARS-CoV-2 entry?Cytokine · 2021Article
- SARS-CoV-2 Entry Genes Expression in Relation with Interferon Response in Cystic Fibrosis Patients.Microorganisms · 2021Article
- Type I interferons can be detected in respiratory swabs from SARS-Cov-2 infected patients.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2020Article
- Clinical and biological consequences of respiratory syncytial virus genetic diversity.Therapeutic advances in infectious diseaseReview
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchiolitis severity is determined by a complex interaction among viral replication and antiviral immunity. The current respiratory syncytial virus (RSV)-A, genotype ON1 demonstrated a high replicative capacity but seemed to be clinically less severe than the previously circulating RSV-A, NA1. To learn insights about ON1 innate immune response, we analyzed expression levels of type I/III interferon (IFN)-related genes in the respiratory mucosa of infants with RSV bronchiolitis. We enrolled RSV-positive bronchiolitis patients over 12 epidemic seasons at a university hospital in Rome. From nasopharyngeal washings' cells (46 positive to NA1, 47 to ON1 and 28 to RSV-B, genotype BA), the mRNA copy number of the type III IFN receptor (IFNLR1 and IL10RB subunits), and of the type I/III IFN-stimulated genes, MxA and ISG56, was calculated using the threshold cycle relative quantification method with respect to an invariant gene. Expression levels of type III IFN receptor subunits genes positively correlated to each other and did not differ in infants infected with different RSV genotypes. The ISGs levels also positively correlated between them but differed among groups. MxA levels were significantly higher in NA1-infected infants than in those with ON1 and BA; ISG56 expression was slightly higher in NA1 than in the other strains. Interestingly, a moderate negative correlation existed between viral load and both ISGs values in ON1-infected infants only. The reduced ISG levels elicited during infections with ON1 (and BA) may cause a weaker control of RSV replication and/or an inadequate host immune response which may impact the risk of respiratory sequelae.
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