HPV replicative cycle and role of viral proteins in lesion progression

Abstract

Human papillomaviruses are DNA viruses that primarily infect the stratified squamous epithelium of the genital tract mucosa. Some of these viruses are strongly associated with cervical cancer. They are sexually transmitted agents that are highly prevalent around the world. Most infections heal spontaneously, in approximately 18 to 24 months, but in some individuals, the virus persists in a latent, asymptomatic form or a productive form, causing cervical intraepithelial lesions that may progress to result in invasive cervical cancer. During productive infection, the virus executes a complex interaction program with the host cell dependent on differentiation and, through its proteins, nullifies the host cell's protective mechanisms against malignant transformation and suppresses the host's immune responses. Initial lesions may spontaneously revert, but those that reach a certain stage, if not treated, progress to malignant forms. In this review, we present some advances in the biology of HPV infection and the role of its proteins in the interaction with the host cell and its consequences.