[Human papillomavirus and the development of cervical cancer: concept of carcinogenesis]. 
Infection with high risk human papillomavirus (hrHPV) plays a central aetiological role in cervical cancer.  Still, cervical carcinogenesis is a multistep process which requires other events in addition to hrHPV infection.  Recent data have resulted in the following concept of cervical carcinogenesis: hrHPV infects normal squamous epithelium.  In most cases this will not lead to a lesion or at worst give rise to a regressing low grade cervical intraepithelial neoplasia (CIN).  Both phenomena involve viral clearance.  Only persistent hrHPV infections will lead to a high grade CIN lesion, a subset of which may undergo malignant transformation.  At the transition of CIN 2 to CIN 3 deregulated expression of the viral oncogenes E6 and E7 takes place, resulting in genetic instability.  Subsequently, activation of the telomere-lengthening enzyme, telomerase occurs, at the result of which cells obtain an infinite replication capacity.  Ultimately, successive allele losses occur at different chromosomal locations which, followed by a clonal outgrowth result in an invasive carcinoma.