The pathobiology and mechanisms of infection of HPV
Wood, N.H.; Khammissa, R.A.G.; Chikte, U.M.E.; Meyerov, R.; Lemmer, J.; Feller, L.
Sadj Journal of the South African Dental Association 65(3): 124-126
2010
ISSN/ISBN: 1029-4864 PMID: 20496845 Document Number: 641871
There are more than 120 types of low-risk and high-risk human papillomaviruses, all of which are epitheliotropic. HPV infection may be latent, or active in a subclinical form or a symptomatic form, the latter manifesting as benign or malignant neoplasms. In basal cells with non-productive HPV infection some early HPV proteins are expressed independently of cell maturation: the productive cycle of HPV replication depends upon specific cellular factors of the maturation of the infected keratinocytes. In HPV-mediated oncogenesis, the combined pathobiological effects of E6 and E7 oncoproteins of high-risk HPV culminate in cellular genomic instability and transformation of persistently infected cells, that progress to the development of a malignant phenotype. In this article we provide insights into the stages of HPV infection, and into the viral genomic organization and replicative cycle.