Mechanistic and epidemiological evidence on the relationship between microbiota, virome and carcinogenesis; [Механистические и эпидемиологические данные о роли микробиоты и вирома в канцерогенезе]

Recent development of molecular and genetic technologies has demonstrated at the molecular level the co-evolutionary principles of interaction between microbiota, virome and the host organism, as well as the role of microorganisms and viruses both in maintaining physiological homeostasis and in the development of various diseases, including malignant neoplasms. The presented review is devoted to the analysis and generalization of modern data on microorganisms and viruses inhabiting the human body, their role in the processes of initiation, promotion and progression of carcinogenesis. The review provides information on known oncogenic viruses and microorganisms according to the modern classification of carcinogenic agents of the International Agency for Research on Cancer. Mechanistic data on the procarcinogenic effect of microbiota and virome are considered in accordance with the modern concept of key characteristics of a carcinogenic agent. Particular attention is paid to the analysis of data on the influence of microbiota and virome on the immunity of the host organism, including both the first results of immunotherapy with Coley toxin of soft tissue sarcomas and osteosarcomas, and data on the influence of individual types of microorganisms on the formation of the immunocompetent cell profile of the host organism. In addition, the influence of intratumor and intracellular microbiota, respectively, on the microenvironment of tumor cells and cellular signaling, including in solid tumors that have no contact with the external environment are also discussed. The data presented are important in terms of the holobiota concept, showing the interdependent existence of the human body, microorganisms and viruses, to improve the prevention and therapy of malignant neoplasms. © 2024 ABV-press Publishing House. All rights reserved.