Human papillomavirus and cervical carcinogenesis

Epidemiological studies show that infection with a subset of genital human papillomavirus (HPV) infections is the major risk factor for the subsequent development of cervical cancer. Experimental studies show that that the E6 and E7 genes of these high risk HPVs are oncogenes that deregulate key cel l cycle controls. In the normal infectious cycle high level expression of t hese genes is confined to non-dividing differentiated cells: HPV oncogenesi s requires deregulation of viral and cellular genes permitting inappropriat e expression of E6 and E7. These are rare events but viral persistence and chronic exposure to steroid hormones increase the probability of this dereg ulation.