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Latent Adenoviral Infection in the Pathogenesis of Emphysema*: The Parker B. Francis Lectureship

James C. Hogg, MD, PhD
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*From the University of British Columbia Pulmonary Research Laboratory, St. Paul’s Hospital, Vancouver, British Columbia, Canada.

Correspondence to: James C. Hogg, MD, PhD, University of British Columbia Pulmonary Research Laboratory, St. Paul’s Hospital, 1081 Burrard St, Vancouver, British Columbia, Canada V6Z 1Y6; e-mail: jhogg@prl.pulmonary.ubc.ca



Chest. 2000;117(5_suppl_1):282S-285S. doi:10.1378/chest.117.5_suppl_1.282S-a
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Abbreviations: ALRI = acute lower respiratory tract infection; ICAM = intercellular adhesion molecule; IL = interleukin; RSV = respiratory syncytial virus

Cigarette smoking causes airway and alveolar inflammation in everyone who smokes and is the major risk factor for developing COPD. However, as only 10 to 15% of heavy smokers develop emphysema and airways obstruction,1 other risk factors must influence cigarette smoke-induced lung inflammation to cause the lesions that produce COPD. Several factors that add risk to cigarette smoking have been identified,2 but this brief review is designed to concentrate on lower respiratory tract infections with particular reference to the hypothesis that latent adenoviral infection is capable of amplifying cigarette smoke-induced lung inflammation to produce emphysema.

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