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U ovom radu prikazan je pregled značajnijih vrsta tumorskih virusa koji su podijeljeni s obzirom na osnovnu morfologiju, kemijski sastav i način replikacije. Onkogen je stanični ili virusni gen koji može inducirati transformaciju stanica, a onkogeni virusi su oni koji mogu inducirati tvorbu tumora. Članovi šest različitih obitelji virusa sposobni su izravno uzrokovati zloćudni tumor u životinjama ili ljudima. Virusi, koji pripadaju pet od tih obitelji, imaju DNK genom i nazivaju se DNK tumorskim virusima. Članovi šeste obitelji tumorskih virusa, retrovirusi, imaju RNK genom u virusnim česticama. DNK tumorski virusi su Hepatitis B virus, SV40 i poliomavirus, Papilomavirusi, Adenovirusi i Herpesvirusi, a u RNK tumorske viruse ubrajaju se Retrovirusi. Put od virusne infekcije do onkogeneze je spor i samo mali broj zaraženih osoba napreduje do zloćudnih tumora, budući da primarna infekcija virusom općenito nije dovoljna za zloćudni tumor. A review of the types of tumour viruses is presented in this thesis. Viruses are divided based on basic morphology, chemical composition and replication. Oncogene is a cell or viral gene that can induce cell transformation, and oncogenic viruses are viruses that can induce tumour formation. Members of six different family of viruses are capable of directly causing cancer in animals or humans. Viruses that are part of five of these families have DNA genomes and are called DNA tumour viruses. Members of the sixth family of tumour viruses, retroviruses, have RNA genomes in viral particles. DNA tumour viruses are Hepatitis B virus, SV40 and poliomavirus, Papillomaviruses, Adenoviruses and Herpesviruses, and RNA tumour viruses are Retroviruses. The path from viral infection to tumorigenesis is slow and only a small number of people are progressing to cancer, since primary infection with the virus is generally insufficient for cancer.

Approximately 15-20% of global cancer incidence is causally linked to viral infection, yet the low incidence of cancers in healthy infected individuals suggests that malignant conversion of virus-infected cells occurs after a long period as a result of additional genetic modifications. There are four families of viruses that are now documented to be involved in the development of human cancers which include members of the polyomavirus, hepadnavirus, papillomavirus and herpesvirus families. Although a number of these viruses are implicated in the aetiology of lymphomas or leukaemias, the vast majority are associated with malignancies of epithelial cells. In epithelial tissues, several classes of proteins are involved in maintaining tissue architecture, including those that promote cell-cell adhesion, and others, which mediate cell-matrix interactions. Proteins representative of all classes are frequently altered in malignant tumour cells that possess invasive and metastatic properties. Malignant tumour cells acquire mechanisms to degrade basement membranes and invade the underlying tissue. Many viruses encode proteins which engage signalling pathways that affect one or more of these mechanisms. It is believed that activation of these processes by chronic viral infection can, under certain circumstances, promote tumour cell invasion and metastasis. This review will take a brief look at the current knowledge of viral-induced alterations in cell motility and invasiveness in the context of tumour invasion and metastasis. DNA tumour viruses promote tumour cell invasion and metastasis by deregulating the normal processes of cell adhesion and motility.