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Viruses
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Rhinoviruses and Asthma
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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: closed (30 September 2024) | Viewed by 9856

Special Issue Editor

Dr. Yury A. Bochkov

E-Mail Website
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

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Published Papers (5 papers)

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Research

15 pages, 3606 KiB  
Article
Surfactant Protein A Inhibits Human Rhinovirus C Binding and Infection of Airway Epithelial Cells from Pediatric Asthma
by Sasipa Tanyaratsrisakul, Yury A. Bochkov, Vanessa White, Heejung Lee, Jessica Loeffler, Jamie Everman, Allison M. Schiltz, Kristy L. Freeman, Katharine L. Hamlington, Elizabeth A. Secor, Nathan D. Jackson, Hong Wei Chu, Andrew H. Liu, Julie G. Ledford, Monica Kraft, Max A. Seibold, Dennis R. Voelker and Mari Numata
Viruses 2024, 16(11), 1709; https://doi.org/10.3390/v16111709 - 30 Oct 2024
Viewed by 1411
Abstract
Rhinovirus C (RV-C) infection can trigger asthma exacerbations in children and adults, and RV-C-induced wheezing illnesses in preschool children correlate with the development of childhood asthma. Surfactant protein A (SP-A) plays a critical role in regulating pulmonary innate immunity by binding to numerous [...] Read more.
Rhinovirus C (RV-C) infection can trigger asthma exacerbations in children and adults, and RV-C-induced wheezing illnesses in preschool children correlate with the development of childhood asthma. Surfactant protein A (SP-A) plays a critical role in regulating pulmonary innate immunity by binding to numerous respiratory pathogens. Mature SP-A consists of multiple isoforms that form the hetero-oligomers of SP-A1 and SP-A2, organized in 18-mers. In this report, we examined the efficacy of SP-A to antagonize RV-C infection using the wild-type (RV-C15) and reporter-expressing (RV-C15-GFP) viruses in differentiated nasal epithelial cells (NECs) from asthmatic and non-asthmatic children. We also determined the antiviral mechanism of action of SP-A on RV-C15 infection. The native SP-A was purified from alveolar proteinosis patients. The recombinant (r) SP-A1 and SP-A2 variants were expressed in FreeStyle™ 293-F cells. SP-A reduced the fluorescent focus-forming units (FFUs) after RV-C15-GFP infection of NECs by 99%. Both simultaneous and 4 h post-infection treatment with SP-A inhibited RV-C15 and RV-C15-GFP viral RNA load by 97%. In addition, the antiviral genes and chemokines (IFN-λ, IRF-7, MDA-5, and CXLC11) were not induced in the infected NECs due to the inhibition of RV-C propagation by SP-A. Furthermore, SP-A bound strongly to RV-C15 in a dose- and Ca2+-dependent manner, and this interaction inhibited RV-C15 binding to NECs. In contrast, rSP-A1 did not bind to solid-phase RV-C15, whereas the rSP-A2 variants, [A91, K223] and [P91, Q223], had strong binding affinities to RV-C15, similar to native SP-A. This study demonstrates that SP-A might have potential as an antiviral for RV infection and RV-induced asthma exacerbations. Full article
(This article belongs to the Special Issue Rhinoviruses and Asthma)
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11 pages, 978 KiB  
Article
The Effect of a TLR3 Agonist on Airway Allergic Inflammation and Viral Infection in Immunoproteasome-Deficient Mice
by Niccolette Schaunaman, Taylor Nichols, Diana Cervantes, Paige Hartsoe, Deborah A. Ferrington and Hong Wei Chu
Viruses 2024, 16(9), 1384; https://doi.org/10.3390/v16091384 - 29 Aug 2024
Cited by 2 | Viewed by 1185
Abstract
Allergic asthma is characterized by increased type 2 inflammation, including eosinophils. Subjects with allergic asthma have recurrent symptoms due to their constant exposure to environmental allergens, such as house dust mite (HDM), which can be further exacerbated by respiratory infections like rhinovirus. The [...] Read more.
Allergic asthma is characterized by increased type 2 inflammation, including eosinophils. Subjects with allergic asthma have recurrent symptoms due to their constant exposure to environmental allergens, such as house dust mite (HDM), which can be further exacerbated by respiratory infections like rhinovirus. The immunoproteasome (IP) is a proteolytic machinery that is induced by inflammatory mediators during virus infection, but the role of the IP in airway allergic inflammation during rhinovirus infection remains unknown. Wild-type (WT) and IP knockout (KO) mice were challenged with HDM. At 48 h after the last HDM challenge, mice were infected with rhinovirus 1B (RV-A1B) for 24 h. After HDM and RV-A1B treatment, IP KO (vs. WT) mice had significantly more lung eosinophils and neutrophils, as well as a significantly higher viral load, but less IFN-beta expression, compared to WT mice. A TLR3 agonist polyinosinic-polycytidylic acid (Poly I:C) treatment after RV-A1B infection in HDM-challenged IP KO mice significantly increased IFN-beta expression and reduced viral load, with a minimal effect on the number of inflammatory cells. Our data suggest that immunoproteasome is an important mechanism functioning to prevent excessive inflammation and viral infection in allergen-exposed mice, and that Poly I:C could be therapeutically effective in enhancing the antiviral response and lessening the viral burden in lungs with IP deficiency. Full article
(This article belongs to the Special Issue Rhinoviruses and Asthma)
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21 pages, 4463 KiB  
Article
Human Stimulator of Interferon Genes Promotes Rhinovirus C Replication in Mouse Cells In Vitro and In Vivo
by Monty E. Goldstein, Maxinne A. Ignacio, Jeffrey M. Loube, Matthew R. Whorton and Margaret A. Scull
Viruses 2024, 16(8), 1282; https://doi.org/10.3390/v16081282 - 10 Aug 2024
Cited by 1 | Viewed by 1834
Abstract
Rhinovirus C (RV-C) infects airway epithelial cells and is an important cause of acute respiratory disease in humans. To interrogate the mechanisms of RV-C-mediated disease, animal models are essential. Towards this, RV-C infection was recently reported in wild-type (WT) mice, yet, titers were [...] Read more.
Rhinovirus C (RV-C) infects airway epithelial cells and is an important cause of acute respiratory disease in humans. To interrogate the mechanisms of RV-C-mediated disease, animal models are essential. Towards this, RV-C infection was recently reported in wild-type (WT) mice, yet, titers were not sustained. Therefore, the requirements for RV-C infection in mice remain unclear. Notably, prior work has implicated human cadherin-related family member 3 (CDHR3) and stimulator of interferon genes (STING) as essential host factors for virus uptake and replication, respectively. Here, we report that even though human (h) and murine (m) CDHR3 orthologs have similar tissue distribution, amino acid sequence homology is limited. Further, while RV-C can replicate in mouse lung epithelial type 1 (LET1) cells and produce infectious virus, we observed a significant increase in the frequency and intensity of dsRNA-positive cells following hSTING expression. Based on these findings, we sought to assess the impact of hCDHR3 and hSTING on RV-C infection in mice in vivo. Thus, we developed hCDHR3 transgenic mice, and utilized adeno-associated virus (AAV) to deliver hSTING to the murine airways. Subsequent challenge of these mice with RV-C15 revealed significantly higher titers 24 h post-infection in mice expressing both hCDHR3 and hSTING—compared to either WT mice, or mice with hCDHR3 or hSTING alone, indicating more efficient infection. Ultimately, this mouse model can be further engineered to establish a robust in vivo model, recapitulating viral dynamics and disease. Full article
(This article belongs to the Special Issue Rhinoviruses and Asthma)
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12 pages, 1254 KiB  
Article
Disease Severity and Cytokine Expression in the Rhinovirus-Induced First Wheezing Episode
by Pekka Hurme, Miisa Kähkönen, Beate Rückert, Tero Vahlberg, Riitta Turunen, Tytti Vuorinen, Mübeccel Akdis, Cezmi A. Akdis and Tuomas Jartti
Viruses 2024, 16(6), 924; https://doi.org/10.3390/v16060924 - 7 Jun 2024
Cited by 1 | Viewed by 1418
Abstract
Wheezing children infected with rhinovirus (RV) have a markedly increased risk of subsequently developing recurrencies and asthma. No previous studies have assessed the association between cytokine response and the severity of acute illness in the first wheezing episode in children infected with RV. [...] Read more.
Wheezing children infected with rhinovirus (RV) have a markedly increased risk of subsequently developing recurrencies and asthma. No previous studies have assessed the association between cytokine response and the severity of acute illness in the first wheezing episode in children infected with RV. Forty-seven children treated both as inpatients and as outpatients infected with RV only, aged 3–23 months, with severe first wheezing episodes were recruited. During acute illness, peripheral blood mononuclear cells (PBMCs) were isolated and stimulated with anti-CD3/anti-CD28 in vitro. A multiplex ELISA was used to quantitatively identify 56 different cytokines. The mean age of the children was 17 months, 74% were males, 79% were hospitalized, and 33% were sensitized. In adjusted analyses, the inpatient group was characterized by decreased expressions of interferon gamma (IFN-γ), interleukin 10 (IL-10), macrophage inflammatory protein 1 alpha (MIP-1α), RANTES (CCL5), and tumor necrosis factor-alpha (TNF-α) and an increased expression of ENA-78 (CXCL5) compared to the outpatient group. The cytokine response profiles from the PBMCs were different between the inpatient and outpatient groups. Our results support that firmly controlled interplay between pro-inflammatory and anti-inflammatory responses are required during acute viral infection to absolve the initial infection leading, to less severe illness. Full article
(This article belongs to the Special Issue Rhinoviruses and Asthma)
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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
Cited by 2 | Viewed by 2937
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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