Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Front Cell Infect Microbiol. 2021 Mar 26;11:605258. doi: 10.3389/fcimb.2021.605258. eCollection 2021.
Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are two oncogenic human γ-herpesviruses that are each associated with 1-2% of human tumors. They encode bona fide oncogenes that they express during latent infection to amplify their host cells and themselves within these. In contrast, lytic virus particle producing infection has been considered to destroy host cells and might be even induced to therapeutically eliminate EBV and KSHV associated tumors. However, it has become apparent in recent years that early lytic replication supports tumorigenesis by these two human oncogenic viruses. This review will discuss the evidence for this paradigm change and how lytic gene products might condition the microenvironment to facilitate EBV and KSHV associated tumorigenesis.
爱泼斯坦-巴尔病毒(EBV)和卡波西肉瘤相关疱疹病毒(KSHV)是两种致癌的人类γ疱疹病毒,每种病毒都与 1-2%的人类肿瘤有关。它们编码真正的致癌基因,在潜伏感染期间表达这些基因,以扩增它们在这些细胞中的宿主细胞和自身。相比之下,裂解病毒粒子产生的感染被认为会破坏宿主细胞,甚至可能被诱导用于治疗性消除 EBV 和 KSHV 相关的肿瘤。然而,近年来,早期裂解复制通过这两种人类致癌病毒支持肿瘤发生已变得明显。这篇综述将讨论这一范式转变的证据,以及裂解基因产物如何调节微环境,以促进 EBV 和 KSHV 相关的肿瘤发生。