Persistent HPV infection with an oncogenic strain of high-risk HPV is a necessary risk factor for the development of invasive cervical cancer. The improved understanding of the cytopathic effects of HPV led to the development of novel diagnostic and preventative tools. HPV manages to evade the immune response of the host. Oncogenic HPV infection does not progress to cancer in all infected individuals and certain variables make individuals more susceptible to the development of pre-malignant and malignant disease. The alpha HPV types are divided into high- and low-risk types according to their ability to cause malignant disease. HPV is mostly transmitted by mucosal contact and infects basal keratinocytes, most likely at a site of micro-trauma that exposes the basal layer to virus. The ability of low-risk HPV to disrupt cell proliferation is limited. In high-risk HPV infections, E6 and E7 are expressed early and strongly leading to accumulation of genetic changes that progress to cancer. The specific HPV type is the strongest factor associated with persistence and oncogenic potential. The concept of latency and reactivation may explain the re-emergence of HPV DNA detection many years after exposure. After a period of latency, reactivation of detectable HPV may follow immune suppression or hormonal changes.