Oncogenic viruses are among the apparent causes of cancer-associated mortality. It was estimated that 12% to 15% of human malignancies are linked to oncoviruses. Although modernist strategies and traditional genetic studies have defined host-pathogen interactions of the oncoviruses, their host functions which are critical for the establishment of infection still remain mysterious. However, over the last few years, it has become clear that infections hijack and modify cellular pathways for their benefit. In this context, we constructed the virus-host protein interaction networks of seven oncoviruses (EBV, HBV, HCV, HTLV-1, HHV8, HPV16, and HPV18), and revealed cellular pathways hijacking as a result of oncogenic virus infection. Several signaling pathways/processes such as TGF-β signaling, cell cycle, retinoblastoma tumor suppressor protein, and androgen receptor signaling were mutually targeted by viruses to induce oncogenesis. Besides, cellular pathways specific to a certain virus were detected. By this study, we believe that we improve the understanding of the molecular pathogenesis of viral oncogenesis and provide information in setting new targets for treatment, prognosis, and diagnosis.

致癌病毒是与癌症相关的死亡率的明显原因之一。据估计，人类恶性肿瘤中有12％至15％与癌病毒有关。尽管现代主义策略和传统遗传研究已经定义了癌病毒的宿主-病原体相互作用，但是它们对于建立感染至关重要的宿主功能仍然神秘。然而，在过去的几年中，很明显，感染劫持并改变了细胞途径以利于它们。在此背景下，我们构建了七种癌病毒（EBV，HBV，HCV，HTLV-1，HHV8，HPV16和HPV18）的病毒-宿主蛋白相互作用网络，并揭示了致癌病毒感染导致的细胞途径劫持。几种信号传导途径/过程，例如TGF-β信号传导，细胞周期，成视网膜细胞瘤肿瘤抑制蛋白，病毒将雄激素受体信号和雄激素受体信号转导，共同诱导肿瘤发生。此外，还检测到特定病毒的细胞途径。通过这项研究，我们相信我们将增进对病毒致癌分子发病机理的了解，并为确定治疗，预后和诊断的新靶标提供信息。