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Stephen Man
Figure 1. Human papillomavirus (HPV) infection and replication in cervical epithelial cells. (a) The normal cervix has a (narrow) transformation zone in which there is an abrupt transition from a columnar epithelium (sometimes via a metaplastic epithelium) to a squamous epithelium; HPVs are probably most infectious to cells that are close to this junction. (b) HPV viruses gain access to the basal epithelial cells of the cervix via the vagina (for example, during sexual intercourse), where they replicate episomally (outside the host chromosome in the nucleus) and express the (early) viral genes E1, E2, E4, E5, E6 and E7. (c) The infected basal cells, which show signs of cell disruption as a result of the viral infection, continue their differentiation and migration to the epithelial surface, where (d) the (now) squamous cells start to express the late HPV genes LI and L2. Infectious virus particles are formed and shed into the lumen of the vagina. (e) HPV infection (particularly with the high-risk types) can progress to: (1) HPV-induced mild dysplasia, (2) the final stages of cervical intraepithelial neoplasia (CIN3) and, eventually, (3) invasive cervical cancer (CaCx), when the basement membrane is breached by the cells, allowing local spread and also distant metastasis. (f) In transformed epithelial cells, HPV genes are integrated into the host chromosomes, with expression of (the oncogenic) E6 and E7 proteins, which bind to the tumour-suppressor proteins p53 and Rb (fig001smc).
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