Cupić Maja, Lazarević Ivana, Kuljić-Kapulica Nada
Srp Arh Celok Lek. 2005 Jul-Aug;133(7-8):384-7. doi: 10.2298/sarh0508384c.
Oncogenic viruses trigger persistent infections, which can stimulate uncontrolled cell growth by inducing cell transformation. Different oncogenic viruses use different mechanisms for infecting cells. Most oncogenic DNA viruses integrate transforming sets of genes into the host chromosome and encode proteins that bind and inactivate cell growth regulatory proteins, such as p53 and retinoblastoma gene product. Tumourous RNA viruses use different oncogenic mechanisms. Some of them encode oncogenic proteins that are almost identical to the cellular proteins involved in the control of cellular growth. The overproduction or altered function of these oncogenic materials stimulates cell growth. These RNA viruses can cause tumours rapidly. The second group of oncoviruses integrates their promoter sequences and viral enhancers near to the cellular growth-stimulating gene, initiating the transformation of the cell. The third group of RNA tumour viruses encodes a protein tax that transactivates the expression of cellular genes. Virus-induced malignant transformation of the cell represents the first step in the complex process of oncogenesis.
致癌病毒引发持续性感染，这种感染可通过诱导细胞转化来刺激细胞不受控制地生长。不同的致癌病毒采用不同的机制感染细胞。大多数致癌DNA病毒将转化基因集整合到宿主染色体中，并编码能结合并使细胞生长调节蛋白（如p53和视网膜母细胞瘤基因产物）失活的蛋白质。肿瘤性RNA病毒采用不同的致癌机制。其中一些编码的致癌蛋白与参与细胞生长控制的细胞蛋白几乎相同。这些致癌物质的过量产生或功能改变会刺激细胞生长。这些RNA病毒可迅速引发肿瘤。第二类致癌病毒将其启动子序列和病毒增强子整合到细胞生长刺激基因附近，引发细胞转化。第三类RNA肿瘤病毒编码一种反式激活细胞基因表达的蛋白tax。病毒诱导的细胞恶性转化是肿瘤发生复杂过程的第一步。
