Wang Yaohao, Yu Jingwen, Pei Yonggang
School of Public Health and Emergency Management, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Front Microbiol. 2024 Dec 5;15:1505191. doi: 10.3389/fmicb.2024.1505191. eCollection 2024.
Epstein-Barr virus (EBV) infects more than 90% of the human population worldwide and establishes lifelong infection in hosts by switching between latent and lytic infection. EBV latency can be reactivated under appropriate conditions, leading to expression of the viral lytic genes and production of infectious progeny viruses. EBV reactivation involves crosstalk between various factors and signaling pathways, and the subsequent complicated virus-host interplays determine whether EBV continues to propagate. However, the detailed mechanisms underlying these processes remain unclear. In this review, we summarize the critical factors regulating EBV reactivation and the associated mechanisms. This encompasses the transcription and post-transcriptional regulation of immediate-early (IE) genes, the functions of viral factors on viral DNA replication and progeny virus production, the mechanisms through which viral proteins disrupt and inhibit the host's innate immune response, and the host factors that modulate EBV reactivation. Finally, we explore the potential applications of novel technologies in studying EBV reactivation, providing novel insights into the investigation of mechanisms governing EBV reactivation and the development of anti-EBV therapeutic strategies.
爱泼斯坦-巴尔病毒（EBV）感染了全球90%以上的人口，并通过在潜伏感染和裂解感染之间切换，在宿主体内建立终身感染。EBV潜伏可在适当条件下被重新激活，导致病毒裂解基因的表达和感染性子代病毒的产生。EBV的重新激活涉及多种因素和信号通路之间的相互作用，随后复杂的病毒-宿主相互作用决定了EBV是否继续传播。然而，这些过程背后的详细机制仍不清楚。在这篇综述中，我们总结了调节EBV重新激活的关键因素及其相关机制。这包括立即早期（IE）基因的转录和转录后调控、病毒因子对病毒DNA复制和子代病毒产生的作用、病毒蛋白破坏和抑制宿主固有免疫反应的机制，以及调节EBV重新激活的宿主因素。最后，我们探讨了新技术在研究EBV重新激活中的潜在应用，为研究EBV重新激活的机制和开发抗EBV治疗策略提供了新的见解。
