Published ahead of print on June 15, 2006, doi:10.1165/rcmb.2006-0199TR
American Journal of Respiratory Cell and Molecular Biology. Vol. 35, pp. 513-518, 2006
© 2006 American Thoracic Society DOI: 10.1165/rcmb.2006-0199TR
Role of Viral Infections in Asthma and Chronic Obstructive Pulmonary Disease
David Proud and
Chung-Wai Chow
Airway Inflammation Group and Institute of Infection, Immunity and Inflammation, University of Calgary, Calgary, Alberta; and Division of Respirology, Department of Medicine, University of Toronto, and Toronto General Hospital of the University Health Network, Toronto, Ontario, Canada
Correspondence and requests for reprints should be addressed to David Proud, Ph.D., Professor & Head, Department of Physiology & Biophysics, University of Calgary, HSC 1627, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1 Canada. E-mail: dproud{at}ucalgary.ca
Substantial evidence implicates common respiratory viral infections in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). Children who experience recurrent virally induced wheezing episodes during infancy are at greater risk for developing asthma. In addition, respiratory viral infections are a major trigger for acute exacerbations of both asthma and COPD. Despite the importance of viral infections in asthma and COPD, the mechanisms by which viruses predispose to, or cause exacerbations of, these diseases remain poorly understood. It is clear that viral infections lead to enhanced airway inflammation and can cause airways hyperresponsiveness. The epithelial cell is the principal site of viral infection in the airways and plays a central role in viral modulation of airway inflammation via release of a variety of cytokines, chemokines, and growth factors. The mechanisms by which viral infections modulate epithelial function, therefore, is a topic of intense investigation. The epithelium also contributes to the host innate defense response to viral infection by releasing products that are antiviral and/or can lead to increased recruitment of dendritic cells and lymphocytes. Some evidence supports a role for the epithelial cell in specific immunity, although the response of more conventional cells of the immune system to viral infections is likely the dominant factor in this regard. Although current therapies may help combat virally induced disease exacerbations, they are less than ideal. A better understanding of the mechanisms underlying viral modulation of these diseases, therefore, may lead to new therapeutic approaches.
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