The role of viruses in cell transformation and oncogenesis

The data of modern scientific literature characterizing individual mechanisms of transformation of normal cells and various stages of oncogenesis associated with viruses were analyzed. The data of sequencing of tumor genomes and amino acid sequences indicate that most tumors are a consequence of the accumulation of sequential mutations, a significant contribution to the formation of which was made by oncogenic viruses. Processes that alter or impair the functioning of signaling pathways can contribute to transformation and oncogenesis. The phosphorylation of the ribosomal protein S6 by protein kinase B, which increases the speed, and prolongs the translation time, is critical in oncogenesis. Protein kinase B inhibits the processes of apoptosis, participates in the regulation of the cell cycle, and regulates tissue growth; an increased level of this protein is found in various tumors. Transformation and tumor-associated processes are the result of a combination of dominant mutations with increased function of proto-oncogenes and recessive mutations with a loss of function of tumor suppressor genes encoding proteins that block cell cycle progression. The function of any gene product can be altered by oncogenic viruses. Transforming proteins alter cell proliferation with a limited set of molecular mechanisms. The integration of proviral deoxyribonucleic acid in a specific region of the cellular genome contributes to the induction of tumor-associated processes by non-transductive viruses. Cellular oncogenes induce signaling at various stages of the cell cycle, which ultimately leads to its dysregulation and progression. In cell transformation, the interaction of E1A viral proteins with tumor suppressors RB, histone acetyltransferase p300/CVR, and inhibitors of cyclin-dependent kinases p27 and p21 is crucial. Virus-transforming proteins have various properties, from changing the sequences of primary amino acids to inducing various variants of biochemical activity. Most tumors induced by non-transductive retroviruses result from increased transcription of cellular genes (myc) located in close proximity to integrated proviruses. Latent membrane protein 1 is an integral protein of the plasma membrane and functions as a constitutively active receptor and facilitates the transition from a latent course of infection to a lytic one. In the absence of a ligand, this protein oligomerizes, and activates proteins that control cell proliferation and survival.