Abstract

Background: Epidemiological and molecular biological data suggest that papilloma viruses of the beta genus are capable of causing the development of a number of epithelial non-melanocytic skin neoplasms. One of the most probable hypotheses of the influence of cutaneous human papillomaviruses is of great interest, in which they are considered as a cofactor for the promotion of tumor growth of cells already damaged by tumor-initiating epigenetic factors the result of cumulative ultraviolet-induced damage (UVI), that is, photoaging. Cutaneous papillomaviruses of the genus beta infect the stratified squamous epithelium of the skin, which determines the spectrum of clinical targets, which are the morphological structures of the skin epidermis. The oncogenic strategy of carcinogenic papillomaviruses is enhanced by a number of mechanisms for increasing the aggressiveness of tumor growth, an important feature of which is integrative virogeny, the process of incorporating the viral genome into the cellular chromosomes of epithelial cells.
 Materials and methods: The article presents the results of our own studies of the incidence and degree of viral load of HPV genus beta DNA in 80 patients (42 patients with dermatogeliosis of IIIIV degrees according to Glogau and epithelial neoplasias, 38 patients without dermatogeliosis) and 40 healthy donors.
 Results: We have demonstrated that high rates of detection of papillomaviruses in proliferating tissue identified in immunosuppressive patients with catastrophic manifestations of dermatogeliosis and multiple epithelial neoplasias (papillomas, fibroepitheliomas, keratomas, skin carcinomas) significantly exceed the viral load of virus DNA in normal skin (1.42 0.6 log) and correlate with other clinical and anamnestic signs, in particular, pronounced signs of dermatogeliosis according to Glogau (IV catastrophic stage) and a constitutionally high degree of photosensitivity (IIIII according to Fitzpatrick), which indicates the formation of a "pathological tandem", which is local immunosuppression and multiple proliferative foci of the epidermis.

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