Viral infections and asthma: An inflammatory interface?

Oliver, BGG; Robinson, P; Peters, M; Black, J

Viral infections and asthma: An inflammatory interface?

Oliver, BGG

Robinson, P Peters, M Black, J

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Publication Type:: Journal Article
Citation:: European Respiratory Journal, 2014, 44 (6), pp. 1666 - 1681
Issue Date:: 2014-01-01

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Field	Value	Language
dc.contributor.author	Oliver, BGG https://orcid.org/0000-0002-7122-9262	en_US
dc.contributor.author	Robinson, P	en_US
dc.contributor.author	Peters, M	en_US
dc.contributor.author	Black, J	en_US
dc.date.available	2020-05-25T19:21:21Z
dc.date.issued	2014-01-01	en_US
dc.identifier.citation	European Respiratory Journal, 2014, 44 (6), pp. 1666 - 1681	en_US
dc.identifier.issn	0903-1936	en_US
dc.identifier.uri	http://hdl.handle.net/10453/37810
dc.description.abstract	© 2014 ERS. Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and β<inf>2</inf>-adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, β<inf>2</inf>-adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy.	en_US
dc.relation.ispartof	European Respiratory Journal	en_US
dc.relation.isbasedon	10.1183/09031936.00047714	en_US
dc.subject.classification	Respiratory System	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Respiratory Tract Infections	en_US
dc.subject.mesh	Virus Diseases	en_US
dc.subject.mesh	Asthma	en_US
dc.subject.mesh	Disease Progression	en_US
dc.subject.mesh	Inflammation	en_US
dc.subject.mesh	Adrenal Cortex Hormones	en_US
dc.subject.mesh	Bronchodilator Agents	en_US
dc.subject.mesh	Anti-Inflammatory Agents	en_US
dc.subject.mesh	Adrenergic beta-2 Receptor Agonists	en_US
dc.title	Viral infections and asthma: An inflammatory interface?	en_US
dc.type	Journal Article
utslib.citation.volume	6	en_US
utslib.citation.volume	44	en_US
utslib.for	1103 Clinical Sciences	en_US
utslib.for	1116 Medical Physiology	en_US
utslib.for	110203 Respiratory Diseases	en_US
utslib.for	11 Medical and Health Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	open_access
pubs.issue	6	en_US
pubs.publication-status	Published	en_US
pubs.volume	44	en_US

Abstract:

© 2014 ERS. Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and β2-adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, β2-adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/37810