Папиломавируси. HPV-индуцирана канцерогенеза.

Skin-mucosal warts are mainly benign growths and have been known to humans for centuries. In 1894, C. de Fine-Licht and G. Variot demonstrated their infectious nature. In 1932, Richard Shope isolated the first papillomavirus from rabbits, proving that benign growths could progress to malignant tumors, which led to the development of the multistage theory of carcinogenesis. Human papillomavirus (HPV) infection causes around 5% of all malignant tumors and is associated with 30% of virus-induced cancers. Following HPV infection of basal keratinocytes or cells in the ecto- endocervical transition zone, the viral nucleic acid remains in the cell as episomal DNA. In most cases, infected cells are cleared by the immune system. However, sometimes this does not occur, and the infection becomes chronic. HPV replication in dividing epithelial cells is accompanied by increased expression of the oncogenic proteins E6 and E7. These proteins are responsible for genomic instability, disruption of the cell cycle, cellular proliferation, and malignant transformation of infected cells. Additionally, they induce immune suppression, preventing the immune system from recognizing HPV- infected and transformed cells. Integration of viral DNA into the host genome leads to elevated expression of E6 and E7, promoting HPV-associated malignant transformation of the infected cell.