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Original Research: COPD |

Upper-Respiratory Viral Infection, Biomarkers, and COPD Exacerbations

Omar Kherad, MD; Laurent Kaiser, MD; Pierre-Olivier Bridevaux, MD; François Sarasin, MD; Yves Thomas, PhD; Jean-Paul Janssens, MD; Olivier T. Rutschmann, MD
Author and Funding Information

From the Department of Internal Medicine (Dr Kherad); Central Laboratory of Virology (Drs Kaiser and Thomas), Division of Infectious Diseases; Division of Pulmonary Diseases (Drs Bridevaux and Janssens); and Department of Community and Primary Care Medicine (Drs Sarasin and Rutschmann), Geneva’s University Hospitals and University of Geneva, Geneva, Switzerland.

Correspondence to: Omar Kherad, MD, Department of Internal Medicine, Geneva’s University Hospitals, and Faculty of Medicine, 4 Rue Gabrielle Perret-Gentil 1211, Geneva 14, Switzerland; e-mail: omarkherad@gmail.com


Funding/Support: This work was performed at Geneva’s University Hospitals and Faculty of Medicine, University of Geneva, and was supported by the Pulmonary League of Geneva, Geneva’s University Hospitals, and a grant of the Swiss National Science Foundation attributed to Dr Kaiser (3200B-101670).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(4):896-904. doi:10.1378/chest.09-2225
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Background:  Respiratory viruses frequently are recovered in the upper-respiratory tract during acute exacerbations of COPD (AECOPD), but their role as contributing pathogens remains unclear. The usefulness of procalcitonin and C-reactive protein as indicators of the presence or absence of viral infection in this setting also needs to be evaluated.

Methods:  The study was of a prospective cohort of patients with COPD admitted to the ED for AECOPD. Reverse transcriptase-polymerase chain reaction (RT-PCR) for 14 respiratory viruses was performed on nasopharyngeal swabs collected at admission and after recovery in stable condition.

Results:  Eighty-six patients (mean age, 72 years; male, 64%) were included. During AECOPD, upper-respiratory viral infections were detected in 44 (51%) patients: picornavirus in 22, metapneumovirus in seven, coronavirus in eight, influenza A/B in two, parainfluenza in two, and respiratory syncytial virus in three. A dual infection was present in three patients. After recovery, viruses were detected in only eight (11%) of 71 patients (P < .001 compared with AECOPD phase). In five of these patients, no virus had been identified during the initial exacerbation, thus suggesting a new viral infection acquired during follow-up. During AECOPD, procalcitonin and C-reactive protein levels did not differ significantly between patients with or without a proven viral infection.

Conclusions:  Prevalence of upper-respiratory viral infection, as detected from nasopharyngeal swab by RT-PCR, is high in AECOPD and low after clinical recovery, suggesting that AECOPD frequently are triggered by viral infections initiated in the upper-respiratory tract. In our study, serum procalcitonin and C-reactive protein did not discriminate virus-associated exacerbations from others.

Trial registration:  clinicaltrials.gov; Identifier: NCT00448604.

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