Vol. 2, Issue 1, Part A (2022)

In addition to chemicals and radiation, another source of mutation is viruses. Viruses are very small 'organisms' that can infect the cells of other animals or plants. However, the diversity and complexity of oncogenic mechanisms raises new questions as to the mechanistic role of viruses in cancer. Classical viral oncogenes have been identified for all tumor-associated viruses. To date, seven viruses; Epstein - Barr virus (EBV), Kaposi's Sarcoma Herpesvirus (KSHV), high-risk Human papilloma viruses (HPV), Merkel Cell Polyomavirus (MCPV), Hepatitis B Viruses (HBV), Hepatitis C Viruses (HCV) and Human T-Lymphotropic Virus type 1 (HTLV1)- have been consistently linked to different types of human cancer, and infections are estimated to account for up to 20% of all cancer cases worldwide. Viral oncogenic mechanisms generally include: generation of genomic instability, increase in the rate of cell proliferation, resistance to apoptosis, alterations in DNA repair mechanisms and cell polarity changes, which often coexist with evasion mechanisms of the antiviral immune response. Viral agents also indirectly contribute to the development of cancer mainly through immunosuppression or chronic inflammation, but also through chronic antigenic stimulation. The paper was aimed to review the oncogenic viruses associated with cancer in human as well as the molecular mechanisms by which the viruses induce cellular transformation and their associated cancers.