Abstract

Aim: Review the literature data on the pathogenetic aspects of the formation of squamous intraepithelial lesions and the role of immunological mechanisms in the formation of this group of cervical diseases. Key Points. Cervical cancer (CC) is a multi-stage process that is often preceded by human papillomavirus (HPV)-associated intraepithelial lesions. The establishment of causal interactions between the virus and malignancy, as well as the study of epidemiological data, leads to the formation of models of cervical carcinogenesis: infection, persistence, progression to the precancerous stage, and finally, cervical cancer. Despite the clear and obvious path of malignancy, as well as the availability of generally available diagnostic methods in the arsenal of a practicing obstetrician-gynecologist, the assessment and prediction of the further development of cervical pathologies in patients of active reproductive age remains difficult. In general, cervical cancer can be considered an excellent model for understanding the staging of malignancy processes, which will be primarily associated with the impact of human papillomavirus infection and changes in the immunological aspects of endo-and exo-cervix. Conclusion. An analysis of sources published in the Cochrane Librare, Google Scolare and PubMed systems was carried out. In recent years, the understanding of human papillomavirus-associated tumor interaction with the host immune system has improved, so the development of new approaches targeting immune checkpoints has sparked interest in the use of immunotherapy in cervical cancer. CC is curable if detected at an early stage. However, reliable diagnostic and prognostic markers related to the physiological and pathological regulation of cervical cancer are currently not available. Therefore, the approach to the treatment of cervical cancer has remained unchanged for several decades, and new diagnostic strategies are currently required, due to the interaction of the immune system and the virus. Keywords: genotyping, apoptosis, cervical neoplasia, polymerase reaction, interleukin-18, tumor necrosis factor alpha, viral load.

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