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Alteration of the nasal responses to influenza virus by tobacco smoke

Noah, Terry L.; Zhou, Haibo; Jaspers, Ilona

Current Opinion in Allergy and Clinical Immunology: February 2012 - Volume 12 - Issue 1 - p 24–31
doi: 10.1097/ACI.0b013e32834ecc80
RHINITIS, SINUSITIS AND UPPER AIRWAY DISEASE: Edited by Ruby Pawankar and David P. Skoner

Purpose of review The purpose of this review is to highlight recent data regarding the impact of exposure to tobacco smoke on influenza virus infection. This is timely because of the continuing pattern for influenza to cause epidemics and pandemics.

Recent findings Experimental animal studies suggest tobacco smoke increases severity of respiratory disease with influenza. The interaction is complex and dependent on dose and chronicity of both virus and smoke exposure. Smoke-induced oxidant stress and suppression of innate immunity are mechanistic factors leading to worse disease. Experiments using human respiratory cells show that tobacco smoke increases viral replication through mechanisms including suppression of antiviral pathways and altered cytokine patterns in cell types with central roles in mucosal innate immunity, such as epithelium, dendritic cells, and natural killer cells. Studies also suggest a role for antioxidant strategies in reducing risk. Human volunteer studies using live attenuated influenza virus as a model appear to corroborate many of these findings.

Summary Exposure to tobacco smoke remains extremely prevalent worldwide. Although avoidance of exposure is a primary goal, it is important to understand the mechanisms underlying increased infection risk with tobacco smoke and other pollutant exposures, so that novel preventive or treatment strategies can be developed.

aDepartment of Pediatrics

bCenter for Environmental Medicine, Asthma and Lung Biology

cDepartments of Pediatrics and Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

Correspondence to Dr Terry L. Noah, Campus Box 7310, University of North Carolina, Chapel Hill, NC 27599-7310, USA. Tel: +1 919 966 1055; fax: +1 919 966 6179; e-mail:

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