HPV viral cycle and cervical cancer development. Human papillomavirus (HPV) gains access to basal cells through microabrassions or by infecting the transformation zone, an abrupt transition from a columnar to a squamous epithelium. Infected cells actively express the early genes E1, E2, E4 and E5. Viral oncoproteins E6 and E7 are expressed in limited amounts due to transcriptional repression exerted by E2. Infected basal cells migrate to the lumen as they differentiate; differentiated epithelial cells express the late capside genes L1 and L2. In subclinical infections or low grade intra-epithelial-lesions (LGSIL) the viral genome replicates as an episome and is encapsidated in the nucleus of the upper layer epithelium cells. Shed viral particles then can infect new zones of epithelium or be sexually transmitted. Only a limited number of infections progress to high grade intra-epithelial-lesions (HGSIL) and cervical carcinoma (CC). The progression of LGSIL to CC is associated with the integration of the HPV genome into the host genome and the loss of transcriptional repression exerted by E2.