Tumors are one of the most important health problems for man and animals in the context of human health protection and food hygiene. It is well known that cancer diseases depend on genetic background and subtle molecular regulation of cell division and can be induced by three groups of carcinogens: biological (i.e. some viruses known as oncogenic viruses), physical and chemical. To date more than 50 various DNA (i.e. herpesviruses, adenoviruses, papillomaviriruses and polyomaviriruses) and RNA (retroviruses) viruses have been well documented as oncogenic viruses. Viruses (i.e. oncogenic herpesviruses and retroviruses) have evolved long-term survival strategies (latency) in the infected host. In the 1970s oncogen v-src of Rous sarcoma virus (RSV) were identified as a factor that can transform the cells of an infected host. At present we know more than 100 viral oncogens (v-jun) and antioncogens (tumor-supressor genes), that compete in cancer induction or supression, respectively. In contrast normal growth promoting genes (the host genes termed protooncogens, c-jun: i.e. growth factors, growth factor receptors and transcriptional factors) have been identified. Thus viral carcinogens can trigger oncogenesis by indirect (i.e. induction of immunosupression in the case of Kaposis’s sarcoma in HIV⁺/AIDS⁺ patients or by modification of host cell genome) or direct (i.e. altering the expression of host cell proteins at the point of viral DNA integration) mechanisms. Different molecular models of the replication of DNA and RNA viruses are essential for oncogenesis development in the infected cells and can influence the frequency of cancer induction. In contrast to RNA viral carcinogens DNA viruses are less efficient in tumor induction because the progeny of RNA viruses are continually being released from the virally transformed cells. In this paper the molecular mechanisms of viral oncogenesis in the context of human (EBV, HPV, HCV, HTLV-1) or animal (RSV, AMV, MDV) viruses is briefly described and discussed.
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