带状疱疹发病机制的研究进展  

The Pathogenesis of Herpes Zoster

作　　者：陈娓[1] 刘军连[1] 

机构地区：[1]解放军第306医院皮肤科,北京100101

出　　处：《中国医学文摘（皮肤科学）》2017年第1期33-38,共6页China Medical Abstracts(Dermatology)

摘　　要：带状疱疹(HZ)是一种由潜伏在人体脊髓背根神经节中的水痘-带状疱疹病毒(VZV)再激活、复制引起的感染性皮肤病。HZ发病机制尚未完全明确,在VZV分子特征和功能方面,沉默即刻早期蛋白(immediate early protein,IE)基因是引起病毒复制、激活的关键;在免疫应答方面,特异性细胞免疫抑制是VZV再激活和发生播散的主要原因。VZV被相关模式识别受体识别后激活信号传导通路,诱导炎症因子的产生发挥抗病毒作用,同时间接激活T淋巴细胞介导的免疫应答,共同引起皮肤和神经组织的损伤,发展为HZ。本文综述了HZ发病机制的研究进展。Herpes zoster（HZ） is an infectious skin disease caused by the reactivation of latent varicella zoster virus in dosral root ganglion varicella zoster virus（VZV） latent in dorsal root ganglion.However,its pathogenesis is not clear yet.In this review,two aspects of the pathogenesis of HZ including the molecular and functional characteristics of VZV and the cellular immune response of the host are discussed.It is confirmed that IE gene silencing and the cellular immune suppression are the main causes of viral reactivation and dissemination.Recognition of VZV by pattern recognition receptor induces the production of proinflammatory cytokines activated by signal transduction pathway to conduct antiviral effects,meanwhile,it activates immune response mediated by T lymphocyte,which are involved in the skin and nerve tissue injury to develop herpes zoster.In this review,the pathogenesis of herpes zoster is summarized.

关 键 词：带状疱疹 水痘-带状疱疹病毒 潜伏感染 激活 T淋巴细胞亚群 免疫应答 

分 类 号：R752.12[医药卫生—皮肤病学与性病学]