The effect of virus-induced cellular transformation on oncogenesis

Abstract

Aim to summarize the scientific data presented in the recent publications on tumor-associated processes induced by viruses. We analyzed 23 international publications devoted to the development and course of tumor-related processes associated with oncogenic viruses.
 The tumor-associated mechanisms are based on the processes of cell transformation, which largely depend on the state of telomeres. No less important are viral and cellular oncogenes, molecular circuits that control cell proliferation. Viral oncogenes encode proteins that increase the concentration of telomerase in the infected cells, and thereby increase the number of cell division cycles. The immune homeostasis, maintaining the integrity of body tissues, is regulated by activating and inhibiting metabolic pathways. The errors in the functioning of these signaling pathways caused by oncogenic viruses can lead to cell transformation and oncogenesis. Guaninenucleotide-binding protein RAS and protein kinase AKT are important components of signaling pathways that contribute to the production of D-type cyclins that control the cell cycle and regulate the activity of metabolic enzymes. Cyclin-dependent kinase is an important factor controlling cell cycles, damage and problems with nucleic acid replication, as well as proper assembly of the mitotic spindle. These processes can be disrupted by the transformation caused by oncogenic viruses. In most cases, viral oncogenes undergo additional changes that contribute to their transformation potential. The transformative activity of viral gene products correlates with binding to specific cellular proteins. In the immunopathogenesis of oncogenesis, an important role belongs to the inactivation of tumor suppressors, and the processes of phosphorylation.