Abstract
BackgroundHPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. We sought to test the hypothesis that cigarette smoking increases HPV infection in an HPV16 serology study of cancer-free individuals.MethodsSubjects were participants in a risk factor study for head and neck cancer, and were required to have no prior history of either HNSCC or any other cancer. Tobacco use and other risk factor data were gathered through interviewer-assisted questionnaires, while serology was conducted in a blinded fashion using a glutathione S-transferase capture enzyme-linked immunosorbent assay (ELISA) to detect antibodies against HPV16 L1, E1, E2, E4, E6 and E7 proteins. The differences in tobacco use by HPV serology were evaluated by ANOVA; and the reported odds ratios and 95% confidence intervals were determined by using unconditional logistic regression.ResultsWe found no overall association of HPV16 serological markers with smoking. However, when the data were stratified by median age, smoking was positively associated with seropositivity for the HPV16 L1 capsid antigen in the younger controls while the older controls were less likely to be HPV16 L1 positive if they smoked (pinteraction < 0.002). There was no similar association of smoking and age with serological response to the early proteins (i.e E6, E7).ConclusionsExposure to HPV16 capsid protein (L1) is increased among relatively younger adults who smoke and diminished among older smokers. However, this pattern is not accompanied by a differential susceptibility for active infection (as determined by the early gene proteins such as E6 and E7) among young and older smokers.
Highlights
Human papillomavirus (HPV) infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium
Of interest to us was the nature of the association of evidence of an immune response to HPV with an individual’s history of tobacco use. We have examined both L1 antibodies, which are formed after exposure to the virus and do not necessarily indicate recent infection, as well as antibodies to early gene products, which effectively signal relatively recent pathological infection, asking whether tobacco smoking is associated with the presence of these HPV biomarkers
There was no association of number of sexual partners, education, age, sex or smoking or drinking history with HPV16 serology in the unadjusted data
Summary
HPV infection is an established risk factor for oropharyngeal cancer, and it has been proposed that cigarette smoking may potentiate HPV infection in the oral epithelium. HPV16 is estimated to account for the majority of cervical cancers and approximately 90% of all of virus-positive head and neck cancers [1], other high-risk HPVs are known to cause both of these cancers [2]. The majority of incident cancers at these sites diagnosed in the United States today are HPV-associated, and current trends suggest that the incidence of HPV16-positive HNSCC will increase markedly in the near term [3]. Recent studies suggest that the population prevalence of any oral HPV in the United States is approximately 6.9% [4], with the prevalence of high-risk HPV16 being much less, estimated at 1-3% [4]. There is currently considerable interest in understanding the factors that contribute, either together or independently, to increase exposure and infection by HPV in the oral cavity and pharynx
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