Jak HPV wysokiego ryzyka indukuje optymalne środowisko dla własnej replikacji w różnicującym się nabłonku

Human papillomaviruses (HPV) are the most common causative agents of harmless human infections, but persistent infection with some types of HPV poses a serious health risk, because they are associated with many cancers, including cervical cancer and an increasing number of head and neck cancers. The replication cycle of HPV is closely dependent on the differentiation of the stratified mucosal epithelium, meaning that the viral genome must be replicated by different mechanisms at different stages of cell differentiation. The establishment of infection and the maintenance of the viral genome occur in proliferating epithelial cells, where the availability of replication factors is optimal for the virus. However, the productive phase of the viral life cycle, including productive replication, late gene expression and virion production, occurs as a result of epithelial differentiation in cells that normally exit the cell cycle. The virus uses a variety of cell signalling pathways, including DNA Damage Response (DDR), to perform productive replication of its own genome. Understanding the mechanisms involved in replication cycle of HPV is needed to establish an appropriate therapeutic approach to combat HPV related diseases.