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Journal of Virology, January 2008, p. 1053-1058, Vol. 82, No. 2
0022-538X/08/$08.00+0 doi:10.1128/JVI.01813-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Michael J. Conway,
Horng-Shen Chen, and
Craig Meyers*
Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033
Received 17 August 2007/ Accepted 26 October 2007
Epidemiological studies suggest that cigarette smoke carcinogens are cofactors which synergize with human papillomavirus (HPV) to increase the risk of cervical cancer progression. Benzo[a]pyrene (BaP), a major carcinogen in cigarette smoke, is detected in the cervical mucus and may interact with HPV. Exposure of cervical cells to high concentrations of BaP resulted in a 10-fold increase in HPV type 31 (HPV31) viral titers, whereas treatment with low concentrations of BaP resulted in an increased number of HPV genome copies but not an increase in virion morphogenesis. BaP exposure also increased HPV16 and HPV18 viral titers. Overall, BaP modulation of the HPV life cycle could potentially enhance viral persistence, host tissue carcinogenesis, and permissiveness for cancer progression.
Published ahead of print on 7 November 2007.
S.A. and M.J.C. contributed equally to this work.
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