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Published ahead of print on February 2, 2006, doi:10.1164/rccm.200509-1489OC
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American Journal of Respiratory and Critical Care Medicine Vol 173. pp. 871-876, (2006)
© 2006 American Thoracic Society
doi: 10.1164/rccm.200509-1489OC


Original Article

Respiratory Syncytial Virus, Airway Inflammation, and FEV1 Decline in Patients with Chronic Obstructive Pulmonary Disease

Tom M. A. Wilkinson, Gavin C. Donaldson, Sebastian L. Johnston, Peter J. M. Openshaw and Jadwiga A. Wedzicha

Academic Unit of Respiratory Medicine, University College London; and Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College, London, United Kingdom

Correspondence and requests for reprints should be addressed to Professor J.A. Wedzicha, M.D., Academic Unit of Respiratory Medicine, University College London, Royal Free and University College Medical School, Hampstead Campus, Rowland Hill Street, London, NW3 2PF, UK. E-mail: j.a.wedzicha{at}medsch.ucl.ac.uk

Background: Respiratory syncytial virus (RSV) is increasingly recognized as an important pathogen in adults with cardiopulmonary disease. It has been associated with acute exacerbations of chronic obstructive pulmonary disease (COPD); however, it has also been detected in the lower airway in the stable state, but the consequences of RSV in stable disease have not previously been determined. We therefore studied the consequences of RSV persistence in adults with COPD and its effect on airway inflammation and lung function decline.

Methods: A total of 241 sputum samples from 74 patients with COPD (FEV1% predicted, 39.2%; interquartile range, 29.6–57.8%) were collected quarterly in the stable state over 2 yr. RSV was detected by polymerase chain reaction (PCR), quantitative microbiology was performed, and inflammatory cytokines were quantified by ELISA.

Results: RSV RNA was detected in 32.8% of sputum samples. Patients in whom RSV was more frequently detected (> 50% of samples RSV PCR-positive, n = 18) had higher airway inflammation and faster FEV1 decline over the study (101.4 ml/yr [95% confidence interval, 57.1–145.8]) compared with those with less frequent detection of RSV (n = 56; 51.2 ml/yr [31.7–70.8]; p = 0.01). The observed relationship between RSV detection and accelerated lung function decline was independent of smoking status, exacerbation frequency, and lower airway bacterial load.

Conclusions: Persistent RSV detection in patients with COPD is associated with airway inflammation and accelerated decline in FEV1. Chronic RSV infection may be a novel therapeutic target to alter the natural history of COPD.

Key Words: chronic obstructive pulmonary disease • respiratory syncytial virus • FEV1 decline




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