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* From the McDonald Research Laboratory, St. Pauls Hospital, Vancouver, BC, Canada.
Correspondence to: Shizu Hayashi, PhD, McDonald Research Laboratory, St. Pauls Hospital, 1081 Burrard St, Vancouver, BC, Canada V6Z 1Y6; e-mail: shayashi{at}mrl.ubc.ca
We have concentrated on the adenovirus as the source of the heightened inflammatory response of the lungs of patients with COPD. We have concentrated in particular on the responses to agents such as lipopolysaccharides and environmental particulates that contaminate the air we breathe, and we have accumulated evidence that the E1A gene of this virus could be the key player in this process. As other intracellular pathogens such as Chlamydia pneumoniae have recently been implicated in the pathogenesis of COPD, our studies on the adenovirus E1A could serve as the model for investigating the interaction between host and extrinsic factors in the chronic progression of this debilitating lung disease.
Key Words: adenovirus COPD latent infection viral DNA
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