Relevance of the problem of treatment and prophylaxis of cervical diseases associated with HPV is primarily due to the ability of the virus to initiate a malignant transformation.
Papillomavirus infection (PVI) is the most common sexually transmitted infection - more than 50% of the sexually active population is infected with HPV during their lifetime.
Infection of cervical tissues with high-risk human papillomavirus (HR-HPV) is a key etiopathogenetic factor in the occurrence of cervical cancer (CC). HPV has about 100 serotypes and is detected in more than 95% of precancerous lesions and cases of CC. HPV serotypes are divided into high-and low-risk oncogenic serotypes (according to the frequency and significance of the association with the development of cervical precancerous lesions).
HPV infections in young women are mostly transient with the virus being eliminated by own immune response of the body. If a precancerous lesion occurs, but the virus is eliminated due to the immune response, then the neo-plastic process regresses in the future (fig. 11.1, 11.2). About 50% of cases of mild cervical intraepithelial neoplasia (CIN) lesions regress, and only 10% transit to progression in young women. Sexually active women under 30 years of age have a very high rate of HPV infection, while women after 30 years of age have a much lower rate of infection.
It is important to note that HPV infection is a necessary, but insufficient factor for the development of cervical neoplastic process. Persistence of onco-genic HPV types is a necessary, but not the only condition for the development of CC and precancerous lesions. To properly understand the nature of pathogenesis and pathogenetic prevention and treatment of cervical diseases associated with HPV, it is advisable to focus on understanding the stages of PVI development and key molecular mechanisms that implement carcino-genesis in HPV.