Rhinoviruses and Asthma

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 1 May 2024 | Viewed by 1593

Special Issue Editor


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Guest Editor
Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792, USA
Interests: rhinoviruses; epidemiology; molecular diagnostics; immune response; vaccines

Special Issue Information

Dear Colleagues,

Rhinoviruses (RVs) are non-enveloped, positive-strand RNA viruses in the genus Enterovirus of the Picornaviridae family, currently classified into 3 species (RV-A, B and C) and 169 types. They replicate their genome and produce progeny in the epithelial cells of human upper and lower respiratory tracts. RVs are among the most frequent causes of viral infections in humans. They can cause a variety of illnesses, including the common cold, lower respiratory tract illnesses such as bronchitis and pneumonia, and exacerbations of asthma, cystic fibrosis and chronic obstructive pulmonary disease. There are currently no specific treatment or prevention options for RV infection. Since the discovery of RVs in the 1950s, clinical isolates of RV-A and RV-B were classified into 100 serotypes in 1987. The third species remained undetected until 2006, because RV-C does not propagate in the cell lines commonly used for virus isolation in vitro due to its lack of cellular receptor expression. RV-A and RV-C isolates are more virulent in children and are more likely to cause exacerbations of childhood asthma compared to RV-B. RV-induced wheezing illnesses in infancy are strongly associated with a high risk of developing asthma in genetically predisposed children; however, the pathogenic mechanisms underlying both asthma inception and exacerbation are not completely understood. This Special Issue welcomes the submission of research and review papers that focus on different aspects of RV biology and its contribution to pathogenesis of asthma, including phylogenetic analysis and epidemiology of RV infections, novel diagnostic methods, virus–host interactions, virus structure and host immune responses, as well as the development of vaccines and antivirals.

Dr. Yury A. Bochkov
Guest Editor

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Keywords

  • rhinovirus
  • epidemiology
  • phylogenetic analysis
  • immune response
  • antibodies
  • vaccines
  • antivirals
  • asthma
  • exacerbations

Published Papers (1 paper)

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Research

12 pages, 1542 KiB  
Article
Poly I:C Pre-Treatment Induced the Anti-Viral Interferon Response in Airway Epithelial Cells
by Hannah Mitländer, Zuqin Yang, Susanne Krammer, Janina C. Grund, Sabine Zirlik and Susetta Finotto
Viruses 2023, 15(12), 2328; https://doi.org/10.3390/v15122328 - 27 Nov 2023
Viewed by 1076
Abstract
Type I and III interferons are among the most important antiviral mediators. Increased susceptibility to infections has been described as being associated with impaired interferon response in asthmatic patients. In this work, we focused on the modulation of interferon dysfunction after the rhinovirus [...] Read more.
Type I and III interferons are among the most important antiviral mediators. Increased susceptibility to infections has been described as being associated with impaired interferon response in asthmatic patients. In this work, we focused on the modulation of interferon dysfunction after the rhinovirus infection of airway epithelial cells. Therefore, we tested polyinosinic:polycytidylic acid (poly I:C), a TLR3 agonist, as a possible preventive pre-treatment to improve this anti-viral response. In our human study on asthma, we found a deficiency in interferon levels in the nasal epithelial cells (NEC) from asthmatics at homeostatic level and after RV infection, which might contribute to frequent airway infection seen in asthmatic patients compared to healthy controls. Finally, pre-treatment with the immunomodulatory substance poly I:C before RV infection restored IFN responses in airway epithelial cells. Altogether, we consider poly I:C pre-treatment as a promising strategy for the induction of interferon response prior to viral infections. These results might help to improve current therapeutic strategies for allergic asthma exacerbations. Full article
(This article belongs to the Special Issue Rhinoviruses and Asthma)
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