Department of Molecular Virology, Adam Mickiewicz University, Umultowska 89, 61-614, Poznan, Poland.
Clin Epigenetics. 2011 Aug;2(2):233-47. doi: 10.1007/s13148-011-0026-6. Epub 2011 Mar 23.
About 15-20% of human cancers worldwide have viral etiology. Emerging data clearly indicate that several human DNA and RNA viruses, such as human papillomavirus, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, hepatitis B virus, hepatitis C virus, and human T-cell lymphotropic virus, contribute to cancer development. Human tumor-associated viruses have evolved multiple molecular mechanisms to disrupt specific cellular pathways to facilitate aberrant replication. Although oncogenic viruses belong to different families, their strategies in human cancer development show many similarities and involve viral-encoded oncoproteins targeting the key cellular proteins that regulate cell growth. Recent studies show that virus and host interactions also occur at the epigenetic level. In this review, we summarize the published information related to the interactions between viral proteins and epigenetic machinery which lead to alterations in the epigenetic landscape of the cell contributing to carcinogenesis.
全世界约有 15-20%的人类癌症具有病毒病因。新出现的数据清楚地表明，几种人类 DNA 和 RNA 病毒，如人乳头瘤病毒、Epstein-Barr 病毒、卡波济肉瘤相关疱疹病毒、乙型肝炎病毒、丙型肝炎病毒和人类 T 细胞嗜淋巴细胞病毒，有助于癌症的发展。人类肿瘤相关病毒已经进化出多种分子机制来破坏特定的细胞途径，以促进异常复制。虽然致癌病毒属于不同的家族，但它们在人类癌症发展中的策略有许多相似之处，涉及靶向调节细胞生长的关键细胞蛋白的病毒编码致癌蛋白。最近的研究表明，病毒和宿主之间的相互作用也发生在表观遗传水平。在这篇综述中，我们总结了已发表的关于病毒蛋白与表观遗传机制相互作用的信息，这些相互作用导致细胞表观遗传景观的改变，从而促进致癌作用。
