Jones Clinton
College of Veterinary Medicine, Department of Veterinary Pathobiology, Oklahoma State University, Stillwater, OK 74078, USA.
Curr Clin Microbiol Rep. 2023 Dec;10(4):236-245. doi: 10.1007/s40588-023-00202-9. Epub 2023 Jul 27.
Numerous studies concluded stress (acute, episodic acute, or chronic) increases the incidence of human alpha-herpes virus 1 (HSV-1) reactivation from latency in neurons. This review will summarize how stress stimulates viral gene expression, replication, and reactivation from latency.
Stress (capital S) stress-mediated activation of the glucocorticoid receptor (GR) accelerates reactivation from latency, whereas a corticosteroid-specific antagonist impairs viral replication and reactivation from latency. GR and specific stress-induced cellular transcription factors also stimulate viral promoters that drive expression of key viral transcriptional regulators: infected cell protein 0 (ICP0), ICP4, ICP27 and viral tegument protein (VP16). Hence, GR is predicted to initially stimulate viral gene expression. GR-mediated immune-inhibitory functions are also predicted to enhance viral replication and viral spread.
Identifying cellular factors and viral regulatory proteins that trigger reactivation from latency in neurons may provide new therapeutic strategies designed to reduce the incidence of reactivation from latency.
大量研究得出结论，应激（急性、发作性急性或慢性）会增加人类α-疱疹病毒1型（HSV-1）从神经元潜伏状态重新激活的发生率。本综述将总结应激如何刺激病毒基因表达、复制以及从潜伏状态重新激活。
应激（大写S）应激介导的糖皮质激素受体（GR）激活加速了从潜伏状态的重新激活，而一种皮质类固醇特异性拮抗剂会损害病毒复制和从潜伏状态的重新激活。GR和特定应激诱导的细胞转录因子还会刺激病毒启动子，这些启动子驱动关键病毒转录调节因子的表达：感染细胞蛋白0（ICP0）、ICP4、ICP27和病毒被膜蛋白（VP16）。因此，预计GR最初会刺激病毒基因表达。GR介导的免疫抑制功能也预计会增强病毒复制和病毒传播。
识别触发神经元潜伏状态重新激活的细胞因子和病毒调节蛋白，可能会提供旨在降低潜伏状态重新激活发生率的新治疗策略。
