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      Bronchiolitis needs a revisit: Distinguishing between virus entities and their treatments

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          Abstract

          Current data indicate that the “bronchiolitis” diagnosis comprises more than one condition. Clinically, pathophysiologically, and even genetically three main clusters of patients can be identified among children suffering from severe bronchiolitis (or first wheezing episode): (a) respiratory syncytial virus (RSV)‐induced bronchiolitis, characterized by young age of the patient, mechanical obstruction of the airways due to mucus and cell debris, and increased risk of recurrent wheezing. For this illness, an effective prophylactic RSV‐specific monoclonal antibody is available; (b) rhinovirus‐induced wheezing, associated with atopic predisposition of the patient and high risk of subsequent asthma development, which may, however, be reversed with systemic corticosteroids in those with severe illness; and (c) wheeze due to other viruses, characteristically likely to be less frequent and severe. Clinically, it is important to distinguish between these partially overlapping patient groups as they are likely to respond to different treatments. It appears that the first episode of severe bronchiolitis in under 2‐year‐old children is a critical event and an important opportunity for designing secondary prevention strategies for asthma. As data have shown bronchiolitis cannot simply be diagnosed using a certain cutoff age, but instead, as we suggest, using the viral etiology as the differentiating factor.

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          Wheezing rhinovirus illnesses in early life predict asthma development in high-risk children.

          Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood. To define the relationship between specific viral illnesses and early childhood asthma development. A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase-polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed. Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age. Among outpatient viral wheezing illnesses in infancy and early childhood, those caused by RV infections are the most significant predictors of the subsequent development of asthma at age 6 years in a high-risk birth cohort.
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            Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

            Rhinoviruses are the major trigger of acute asthma exacerbations and asthmatic subjects are more susceptible to these infections. To investigate the underlying mechanisms of this increased susceptibility, we examined virus replication and innate responses to rhinovirus (RV)-16 infection of primary bronchial epithelial cells from asthmatic and healthy control subjects. Viral RNA expression and late virus release into supernatant was increased 50- and 7-fold, respectively in asthmatic cells compared with healthy controls. Virus infection induced late cell lysis in asthmatic cells but not in normal cells. Examination of the early cellular response to infection revealed impairment of virus induced caspase 3/7 activity and of apoptotic responses in the asthmatic cultures. Inhibition of apoptosis in normal cultures resulted in enhanced viral yield, comparable to that seen in infected asthmatic cultures. Examination of early innate immune responses revealed profound impairment of virus-induced interferon-β mRNA expression in asthmatic cultures and they produced >2.5 times less interferon-β protein. In infected asthmatic cells, exogenous interferon-β induced apoptosis and reduced virus replication, demonstrating a causal link between deficient interferon-β, impaired apoptosis and increased virus replication. These data suggest a novel use for type I interferons in the treatment or prevention of virus-induced asthma exacerbations.
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              Role of deficient type III interferon-lambda production in asthma exacerbations.

              Rhinoviruses are the major cause of asthma exacerbations, and asthmatics have increased susceptibility to rhinovirus and risk of invasive bacterial infections. Here we show deficient induction of interferon-lambdas by rhinovirus in asthmatic primary bronchial epithelial cells and alveolar macrophages, which was highly correlated with severity of rhinovirus-induced asthma exacerbation and virus load in experimentally infected human volunteers. Induction by lipopolysaccharide in asthmatic macrophages was also deficient and correlated with exacerbation severity. These results identify previously unknown mechanisms of susceptibility to infection in asthma and suggest new approaches to prevention and/or treatment of asthma exacerbations.
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                Author and article information

                Contributors
                tuomas.jartti@utu.fi
                Journal
                Allergy
                Allergy
                10.1111/(ISSN)1398-9995
                ALL
                Allergy
                John Wiley and Sons Inc. (Hoboken )
                0105-4538
                1398-9995
                25 November 2018
                January 2019
                : 74
                : 1 ( doiID: 10.1111/all.2019.74.issue-1 )
                : 40-52
                Affiliations
                [ 1 ] Department of Pediatrics Turku University Hospital and University of Turku Turku Finland
                [ 2 ] Department of Parasitology Leiden University Medical Center Leiden The Netherlands
                [ 3 ] COPSAC Copenhagen Prospective Studies on Asthma in Childhood, Herlev and Gentofte Hospital University of Copenhagen Copenhagen Denmark
                [ 4 ] Department of Pediatric Allergy Istanbul Medeniyet University Göztepe Training and Research Hospital Istanbul Turkey
                [ 5 ] Astrid Lindgren Children's Hospital Karolinska University Hospital Stockholm Sweden
                [ 6 ] Department of Women's and Children's Health Karolinska Institutet Stockholm Sweden
                [ 7 ] Department of Medicine Solna Immunology and Allergy Unit Karolinska Institutet Karolinska University Hospital Stockholm Sweden
                [ 8 ] Allergy Department 2nd Pediatric Clinic University of Athens Athens Greece
                [ 9 ] Imperial College Healthcare NHS Trust London UK
                [ 10 ] Division of Infection Immunity & Respiratory Medicine University of Manchester Manchester UK
                [ 11 ] Department of Pediatrics Medical University of Warsaw Warsaw Poland
                [ 12 ] Department of Pediatric Pneumonology and Allergy Medical University of Warsaw Warsaw Poland
                [ 13 ] Pediatric Allergology Department of Pediatrics Dr. von Hauner Children′s Hospital University Hospital German Center for Lung Research (DZL) LMU Munich Munich Germany
                [ 14 ] Centre for Inflammation Research Queen's Medical Research Institute and Child Life and Health University of Edinburgh Edinburgh UK
                [ 15 ] Institute of Laboratory Medicine Philipps Universität Marburg Marburg Germany
                [ 16 ] Universities of Giessen and Marburg Lung Center (UGMLC) Philipps Universität, Marburg German Center for Lung Research (DZL) Marburg Germany
                Author notes
                [*] [* ] Correspondence

                Tuomas Jartti, the Department of Pediatrics, Turku University Hospital, Turku, Finland.

                Email: tuomas.jartti@ 123456utu.fi

                Author information
                http://orcid.org/0000-0003-2748-5362
                http://orcid.org/0000-0001-9279-2890
                http://orcid.org/0000-0003-2003-1018
                http://orcid.org/0000-0002-5747-7032
                http://orcid.org/0000-0001-7745-8624
                http://orcid.org/0000-0003-0422-3570
                http://orcid.org/0000-0003-4989-9769
                http://orcid.org/0000-0002-4448-3468
                http://orcid.org/0000-0002-3037-6944
                http://orcid.org/0000-0002-6899-748X
                http://orcid.org/0000-0001-5194-5635
                http://orcid.org/0000-0001-6613-2012
                Article
                ALL13624
                10.1111/all.13624
                6587559
                30276826
                418f0d3e-6ed0-44d2-a530-ea352ea0de07
                © 2018 The Authors. Allergy Published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 30 March 2018
                : 07 September 2018
                : 15 September 2018
                Page count
                Figures: 6, Tables: 0, Pages: 13, Words: 8868
                Funding
                Funded by: Universities Giessen and Marburg Lung Center
                Funded by: German Center for Lung Research
                Award ID: 82DZL00502/A2
                Funded by: Deutsche Forschungsgemeinschaft
                Award ID: C04
                Funded by: Sigrid Juselius Foundation, Helsinki, Finland
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                all13624
                January 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.4 mode:remove_FC converted:21.06.2019

                Immunology
                bronchiolitis,respiratory syncytial virus,rhinovirus,virus,wheezing
                Immunology
                bronchiolitis, respiratory syncytial virus, rhinovirus, virus, wheezing

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