For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
1
views
43
references
 Top references
cited by
43
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      696
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      How Viral Infections Cause Exacerbation of Airway Diseases

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Exacerbations of asthma and COPD are major causes of morbidity, mortality, and health-care costs. Over the last decade, studies using new molecular diagnostic techniques have established that respiratory viruses are a major cause of exacerbations of both asthma and COPD. The most prevalent viruses detected during exacerbations are the rhinoviruses. Despite the burden of disease associated with exacerbations, little is known about the mechanisms of virus-induced exacerbations of airway diseases. Exacerbations are associated with increased airway inflammation in patients with both asthma and COPD, but many questions remain unanswered regarding the key inflammatory cells and mediators involved. Identifying the key inflammatory mediators involved in exacerbations holds the promise of developing diagnostic and prognostic markers of exacerbation. In addition, such studies can identify new therapeutic targets for the development of novel drugs for the prevention and treatment of exacerbations.

          Related collections

          Most cited references43

          • Record: found
          • Abstract: found
          • Article: not found

          Community study of role of viral infections in exacerbations of asthma in 9-11 year old children.

          S Johnston, P Pattemore, G. Sanderson … (1995)
          To study the association between upper and lower respiratory viral infections and acute exacerbations of asthma in schoolchildren in the community. Community based 13 month longitudinal study using diary card respiratory symptom and peak expiratory flow monitoring to allow early sampling for viruses. 108 Children aged 9-11 years who had reported wheeze or cough, or both, in a questionnaire. Southampton and surrounding community. Upper and lower respiratory viral infections detected by polymerase chain reaction or conventional methods, reported exacerbations of asthma, computer identified episodes of respiratory tract symptoms or peak flow reductions. Viruses were detected in 80% of reported episodes of reduced peak expiratory flow, 80% of reported episodes of wheeze, and in 85% of reported episodes of upper respiratory symptoms, cough, wheeze, and a fall in peak expiratory flow. The median duration of reported falls in peak expiratory flow was 14 days, and the median maximum fall in peak expiratory flow was 81 l/min. The most commonly identified virus type was rhinovirus. This study supports the hypothesis that upper respiratory viral infections are associated with 80-85% of asthma exacerbations in school age children.
          Article 0 comments Cited 427 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus

            Peter Wark, Sebastian L. Johnston, Fabio Bucchieri … (2005)
            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.
            Article 0 comments Cited 405 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Respiratory viruses, symptoms, and inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease.

              T Seemungal, R. Harper‐Owen, A Bhowmik … (2001)
              The effects of respiratory viral infection on the time course of chronic obstructive pulmonary disease (COPD) exacerbation were examined by monitoring changes in systemic inflammatory markers in stable COPD and at exacerbation. Eighty-three patients with COPD (mean [SD] age, 66.6 [7.1] yr, FEV(1), 1.06 [0.61] L) recorded daily peak expiratory flow rate and any increases in respiratory symptoms. Nasal samples and blood were taken for respiratory virus detection by culture, polymerase chain reaction, and serology, and plasma fibrinogen and serum interleukin-6 (IL-6) were determined at stable baseline and exacerbation. Sixty-four percent of exacerbations were associated with a cold occurring up to 18 d before exacerbation. Seventy-seven viruses (39 [58.2%] rhinoviruses) were detected in 66 (39.2%) of 168 COPD exacerbations in 53 (64%) patients. Viral exacerbations were associated with frequent exacerbators, colds with increased dyspnea, a higher total symptom count at presentation, a longer median symptom recovery period of 13 d, and a tendency toward higher plasma fibrinogen and serum IL-6 levels. Non-respiratory syncytial virus (RSV) respiratory viruses were detected in 11 (16%), and RSV in 16 (23.5%), of 68 stable COPD patients, with RSV detection associated with higher inflammatory marker levels. Respiratory virus infections are associated with more severe and frequent exacerbations, and may cause chronic infection in COPD. Prevention and early treatment of viral infections may lead to a decreased exacerbation frequency and morbidity associated with COPD.
              Article 0 comments Cited 326 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Sebastian L. Johnston
                Journal
                Journal ID (nlm-ta): Chest
                Journal ID (iso-abbrev): Chest
                Title: Chest
                Publisher: The American College of Chest Physicians. Published by Elsevier Inc.
                ISSN (Print): 0012-3692
                ISSN (Electronic): 1931-3543
                Publication date PMC-release: 25 January 2017
                Publication date (Print): October 2006
                Publication date (Electronic): 25 January 2017
                Volume: 130
                Issue: 4
                Pages: 1203-1210
                Affiliations
                [a ]Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, UK
                Author notes
                [* ]Department of Respiratory Medicine, National Heart and Lung Institute and Wright Fleming Institute of Infection & Immunity, Imperial College London, Norfolk Pl, London W2 1PG, UK s.johnston@ 123456imperial.ac.uk
                Article
                Publisher ID: S0012-3692(15)51159-8
                DOI: 10.1378/chest.130.4.1203
                PMC ID: 7172720
                PubMed ID: 17035457
                SO-VID: a2f322fe-eb47-46ca-bd88-2cd737d4a75c
                Copyright © © 2006 The American College of Chest Physicians
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 21 March 2006
                Date accepted : 24 May 2006
                Categories
                Subject: Article

                ScienceOpen disciplines: Respiratory medicine
                Keywords: asthma,copd,exacerbations,viruses,ena, epithelial-derived neutrophil attractant,ifn, interferon,il, interleukin,ltb4, leukotriene b4,nf, nuclear factor,pcr, polymerase chain reaction,rantes, regulated upon activation, normal t-cell expressed and secreted,th, t helper,tlr, toll-like receptor,tnf, tumor necrosis factor
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: asthma, copd, exacerbations, viruses, ena, epithelial-derived neutrophil attractant, ifn, interferon, il, interleukin, ltb4, leukotriene b4, nf, nuclear factor, pcr, polymerase chain reaction, rantes, regulated upon activation, normal t-cell expressed and secreted, th, t helper, tlr, toll-like receptor, tnf, tumor necrosis factor

                Comments

                Comment on this article

                scite_

                Similar content696

                See all similar

                Cited by41

                See all cited by

                Most referenced authors731

                See all reference authors