Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.
Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.
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神经系统中α疱疹病毒潜伏期和发病机制的细胞内在决定因素。
DOI：
10.3390/v15122284
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发表时间：
2023-11-22
期刊：
影响因子：
--
通讯作者：
Koyuncu OO
中科院分区：
文献类型：
--
作者：
Salazar S;Luong KTY;Koyuncu OO
α疱疹病毒感染（α-HV）广泛存在，影响超过70%的成年人群。通常，感染开始于粘膜上皮，病毒颗粒从粘膜上皮侵入周围神经系统的轴突。在外周神经节的细胞核中，α-HV建立终身潜伏期，并最终经历多次再激活周期。在重新激活后，病毒后代可以移动到神经中，回到它们进入生物体的外周，或者它们可以移动到中枢神经系统（CNS）。这种潜伏-再激活循环受到宿主内在和先天免疫应答的复杂作用的控制，并被病毒蛋白质很好地抵消，以努力在群体中共存。如果这种阴阳平衡或纳什平衡样平衡状态由于免疫抑制或宿主反应因子（特别是CNS）的基因突变或其他致病刺激的存在而被打破，则α-HV再激活可能导致危及生命的病理。在这篇综述中，我们将总结从粘膜上皮感染开始的分子病毒-宿主相互作用，导致PNS中潜伏期的建立和α-HV可能的CNS侵袭，突出与NS中病毒复制不受控制相关的病理学。
Alpha herpesvirus infections (α-HVs) are widespread, affecting more than 70% of the adult human population. Typically, the infections start in the mucosal epithelia, from which the viral particles invade the axons of the peripheral nervous system. In the nuclei of the peripheral ganglia, α-HVs establish a lifelong latency and eventually undergo multiple reactivation cycles. Upon reactivation, viral progeny can move into the nerves, back out toward the periphery where they entered the organism, or they can move toward the central nervous system (CNS). This latency–reactivation cycle is remarkably well controlled by the intricate actions of the intrinsic and innate immune responses of the host, and finely counteracted by the viral proteins in an effort to co-exist in the population. If this yin-yang- or Nash-equilibrium-like balance state is broken due to immune suppression or genetic mutations in the host response factors particularly in the CNS, or the presence of other pathogenic stimuli, α-HV reactivations might lead to life-threatening pathologies. In this review, we will summarize the molecular virus–host interactions starting from mucosal epithelia infections leading to the establishment of latency in the PNS and to possible CNS invasion by α-HVs, highlighting the pathologies associated with uncontrolled virus replication in the NS.
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