Lowance Center for Human Immunology, Division of Rheumatology, Departments of Pediatrics and Medicine, Emory University , Atlanta, GA , USA.
Front Immunol. 2014 Jul 22;5:353. doi: 10.3389/fimmu.2014.00353. eCollection 2014.
Human oncogenic viruses include Epstein-Barr virus, hepatitis B virus, hepatitis C virus, human papilloma virus, human T-cell lymphotropic virus, Kaposi's associated sarcoma virus, and Merkel cell polyomavirus. It would be expected that during virus-host interaction, the immune system would recognize these pathogens and eliminate them. However, through evolution, these viruses have developed a number of strategies to avoid such an outcome and successfully establish chronic infections. The persistent nature of the infection caused by these viruses is associated with their oncogenic potential. In this article, we will review the latest information on the interaction between oncogenic viruses and the innate immune system of the host. In particular, we will summarize the available knowledge on the recognition by host pattern-recognition receptors of pathogen-associated molecular patterns present in the incoming viral particle or generated during the virus' life cycle. We will also review the data on the recognition of cell-derived danger associated molecular patterns generated during the virus infection that may impact the outcome of the host-pathogen interaction and the development cancer.
人类致癌病毒包括 Epstein-Barr 病毒、乙型肝炎病毒、丙型肝炎病毒、人乳头瘤病毒、人类 T 细胞嗜淋巴细胞病毒、卡波西肉瘤相关疱疹病毒和 Merkel 细胞多瘤病毒。在病毒-宿主相互作用过程中，免疫系统应该能够识别这些病原体并将其清除。然而，通过进化，这些病毒已经发展出了许多策略来避免这种结果，并成功建立慢性感染。这些病毒引起的持续感染与它们的致癌潜力有关。在本文中，我们将综述致癌病毒与宿主固有免疫系统相互作用的最新信息。特别地，我们将总结宿主模式识别受体识别进入病毒颗粒中的病原体相关分子模式或在病毒生命周期中产生的分子模式的现有知识。我们还将综述关于在病毒感染过程中产生的细胞来源的危险相关分子模式的识别的相关数据，这些数据可能会影响宿主-病原体相互作用的结果以及癌症的发生。
