Malignant tumor is generally defined by the absence of touch inhibition, the possibility of metastasis to other tissues, uncontrolled division and cell proliferation. At least 7 viruses today are known to be associated with tumor formation: hepatitis B virus (HBV) and C virus (HCV), papillomavirus, Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), human T-cell lymphotropic virus (HTLV), human immunodeficiency virus (HIV) and Merkel cell polyomavirus (MCPV). Cell transformation can be affected by viruses: 1) by direct carcinogenesis and 2) by indirect carcinogenesis. Direct carcinogenesis involves the expression of viral oncogenes as well as the deregulation of cellular oncogenes and tumor suppressor genes. In direct carcinogenesis, the genome of the virus can be found in cells isolated from tumor tissue. Indirect carcinogenesis is most often caused by the establishment of chronic inflammation in which the surrounding tissues are constantly damaged by the formation of mutated cells and the fight of the immune system against them. Immunosuppression is another mechanism of indirect tumorigenesis in which the immune system loses the ability to recognize altered cells of its own organism and act against them. An example of direct carcinogenesis are hepressviruses (EBV and KSHV), and for indirect the best example is HIV. Each of the viruses with its infection affects the formation of the associated malignant tumor or more of them. Oncogenic viruses differ from each other in the types of cells they infect, life cycles, the type of molecules that serve as their genetic guide, and all this determines the mechanism by which they will cause the transformation of cells into tumors.