Review

Epithelial maturation and molecular biology of oral HPV

Liviu Feller¹ , Razia AG Khammissa¹ , Neil H Wood¹ and Johan Lemmer^1,2

¹  Department of Periodontology and Oral Medicine, School of Dentistry, University of Limpopo, Medunsa Campus, South Africa

²  Professor Emeritus, Department of Oral Medicine and Periodontology, School of Dentistry, University of the Witwatersrand, Johannesburg, South Africa

author email corresponding author email

Infectious Agents and Cancer 2009, 4:16doi:10.1186/1750-9378-4-16

Published:	25 November 2009

Abstract

Human papillomavirus (HPV) is widespread and can cause latent infection in basal cells, with low HPV DNA copy-number insufficient for transmission of infection; can cause subclinical infection that is active but without clinical signs; or can cause clinical infection leading to benign, potentially malignant or malignant lesions. The HPV cycle is influenced by the stage of maturation of the infected keratinocytes, and the production of virions is restricted to the post-mitotic suprabasal epithelial cells where all the virus genes are expressed.

Low-risk HPV genotypes are associated with the development of benign oral lesions, whereas high-risk HPV genotypes are implicated in the development of malignant epithelial neoplasms. The rôle of high-risk HPV as a causative agent in epithelial malignancy is different at different anatomical sites: it is almost invariably implicated in squamous cell carcinoma of the uterine cervix, fairly frequently implicated in squamous cell carcinoma of the oropharynx, and it is seldom implicated in squamous cell carcinoma of the mouth.