Figure 1

E5 can improve HPV activity by altering host factors controlling the viral replication/persistence. A schematic view of the papillomavirus life cycle highlighting the expression of the HPV genes, which is tightly regulated and strictly linked to epithelial differentiation. E5 could contribute to a successful infection by inducing loss of surface MHC I expression in the infected basal cells preventing presentation of viral antigens to effector T-cells and thus, in addition to other mechanisms of immune avoidance, such as lack of inflammation, contributing to evasion of immune surveillance. Expression of E5 in the basal/suprabasal layers of the epithelium would lead to sustained cell proliferation to favour virus-infected cells, but extinction of its expression in the more superficial layers would permit cell differentiation and virion production. If E5 expression proceeds beyond early lesional stages, keratinocyte differentiation and immunological removal of infected cells would not take place and the lesion would be at greater risk for neoplastic progression. E5 actions on host factors controlling viral replication/persistence are indicated. Dashed dots indicate low levels of E5 gene expression.