Gandhi Jaya, Gaur Nivedita, Khera Lohit, Kaul Rajeev, Robertson Erle S
Department of Microbiology, University of Delhi South Campus, New Delhi, India.
Department of Microbiology, University of Delhi South Campus, New Delhi, India.
Virology. 2015 Oct;484:1-14. doi: 10.1016/j.virol.2015.05.006. Epub 2015 Jun 5.
Inflammation is one of the predisposing factors known to be associated with Epstein Barr Virus (EBV) mediated tumorigenesis. However it is not well understood whether inflammation in itself plays a role in regulating the life cycle of this infectious agent. COX-2, a key mediator of the inflammatory processes is frequently over-expressed in EBV positive cancer cells. In various tumors, PGE2 is the principle COX-2 regulated downstream product which exerts its effects on cellular processes through the EP1-4 receptors. In this study, we further elucidated how upregulated COX-2 levels can modulate the events in EBV life cycle related to latency-lytic reactivation. Our data suggest a role for upregulated COX-2 on modulation of EBV latency through its downstream effector PGE2. This study demonstrates a role for increased COX-2 levels in modulation of EBV latency. This is important for understanding the pathogenesis of EBV-associated cancers in people with chronic inflammatory conditions.
炎症是已知与爱泼斯坦-巴尔病毒（EBV）介导的肿瘤发生相关的诱发因素之一。然而，炎症本身是否在调节这种感染因子的生命周期中发挥作用尚不清楚。COX-2是炎症过程的关键介质，在EBV阳性癌细胞中经常过度表达。在各种肿瘤中，PGE2是COX-2调节的主要下游产物，它通过EP1-4受体对细胞过程发挥作用。在本研究中，我们进一步阐明了COX-2水平上调如何调节与潜伏-裂解再激活相关的EBV生命周期事件。我们的数据表明，上调的COX-2通过其下游效应物PGE2对EBV潜伏的调节作用。本研究证明了COX-2水平升高在调节EBV潜伏中的作用。这对于理解慢性炎症患者中EBV相关癌症的发病机制很重要。
