[Virological and carcinogenic aspects of HPV]

Human papillomaviruses are small viruses belonging to the Papillomaviridae. More than 100 genotypes have been identified, causing benign (low-risk HPV) or malignant (high-risk HPV) cutaneous or mucosal lesions. The low-risk HPV6 and HPV11 provoke genital warts, while the high-risk HPV16 and HPV18 can cause cervical cancer. The HPVgenome includes several open reading frames that encode proteins involved in viral DNA replication (E1 and E2), viral gene expression regulation (E2), virus assembly (E4) and the immortalisation and transformation of infected epithelial cells (E5, E6 and E7; high-risk HPV only). The open reading frames L1 and L2 encode the two capsid proteins. HPV target stem cells of the squamous epithelium. The complete life cycle involves three phases, with sequential expression of viral genes leading to viral DNA replication and to the production of highly infectious virions. Viral DNA integration occurs with high-risk types and leads to the overexpression of two viral oncoproteins, E6 and E7. These proteins, in combination with E5, promote the immortalisation and transformation of infected cells.