The eleven HPV types currently classified as high-risk include: HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, while oncogenic potential of 7 additional HPV types has been suggested in some studies, but not established. There are over 150 types of HPV, which have been categorized into “high-risk” and “low-risk” types based on their potential to induce malignancy in cervical cancer. Further understanding of epidemiology and natural history of the oral HPV infection can inform prevention strategies and screening of oropharynx cancer. Because molecular mechanism, epidemiology, screening and prevention specific to HPV-related oropharynx cancer are reviewed in separate sections of this special issue, we will only briefly summarize the pertinent points in these topics for completeness of this review. In this review, we will highlight lessons learned from investigations of HPV infection of the genital tract and provide insight into interpretation of the current data in prevalence, incidence, natural history, mode of acquisition and risk factors of oral HPV infection.

2- 5 In the U.S., HPV now causes the majority of oropharynx cancer and the total number of the cases is expected to surpass the number of cervical cancers by the year 2020, if the current trend of increasing incidence of oropharynx cancer continues.

The etiologic role of HPV infection in oropharynx cancer has now been firmly established. 1, 2 While the epidemiology, natural history and molecular biology of the HPV infection and subsequent development of cancers in the genital tract have been extensively studied in the past, there are many unknowns in oral HPV infection and its role in development of oropharynx cancer. Human papillomavirus (HPV) infection accounts for approximately 5.2% of the worldwide human cancer burden including the cancers of the anus, genital tract and oropharynx.

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