{"title":"Intimate Relationship Between Stress and Human Alpha‑Herpes Virus 1 (HSV‑1) Reactivation from Latency.","authors":"Clinton Jones","doi":"10.1007/s40588-023-00202-9","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p><p><strong>Summary: </strong>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.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":null,"pages":null},"PeriodicalIF":3.1000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10764003/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Clinical Microbiology Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s40588-023-00202-9","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/7/27 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose of review: 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.
Recent findings: 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.
Summary: 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.
综述的目的:大量研究认为,压力(急性、偶发性急性或慢性)会增加人类α-疱疹病毒1(HSV-1)从神经元潜伏期重新激活的发生率。本综述将总结压力是如何刺激病毒基因表达、复制和从潜伏期重新激活的:最近的研究发现:应激(大写字母 S)介导的糖皮质激素受体(GR)激活可加速潜伏期病毒的重新激活,而皮质激素特异性拮抗剂则会损害病毒复制和潜伏期病毒的重新激活。GR和特定压力诱导的细胞转录因子也会刺激病毒启动子,从而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和病毒外壳蛋白(VP16)。因此,预计 GR 最初会刺激病毒基因的表达。小结:确定引发神经元潜伏期再活化的细胞因素和病毒调控蛋白可能会提供新的治疗策略,以降低潜伏期再活化的发生率。
期刊介绍:
Current Clinical Microbiology Reports commissions expert reviews from leading scientists at the forefront of research in microbiology. The journal covers this broad field by dividing it into four key main areas of study: virology, bacteriology, parasitology, and mycology. Within each of the four sections, experts from around the world address important aspects of clinical microbiology such as immunology, diagnostics, therapeutics, antibiotics and antibiotic resistance, and vaccines. Some of the world’s foremost authorities in the field of microbiology serve as section editors and editorial board members. Section editors select topics for which leading researchers are invited to contribute comprehensive review articles that emphasize new developments and recently published papers of major importance, which are highlighted in annotated reference lists. These timely reviews of the literature examine the latest scientific discoveries and controversies as they emerge and are indispensable to both researchers and clinicians. The editorial board, composed of more than 20 internationally diverse members, reviews the annual table of contents, ensures that topics address all aspects of emerging research, and where applicable suggests topics of critical importance to various countries/regions.