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西尼罗河病毒引起的神经后遗症——与神经退行性级联反应和痴呆症的关系

West Nile Virus-Induced Neurologic Sequelae-Relationship to Neurodegenerative Cascades and Dementias.

作者信息

Vittor Amy Y, Long Maureen, Chakrabarty Paramita, Aycock Lauren, Kollu Vidya, DeKosky Steven T

机构信息

Division of Infectious Disease and Global Medicine, University of Florida, Gainesville, FL, USA.

College of Veterinary Medicine, Department of Comparative, Diagnostic, and Population Medicine, University of Florida, Gainesville, FL, USA.

出版信息

Curr Trop Med Rep. 2020 Mar;7(1):25-36. doi: 10.1007/s40475-020-00200-7. Epub 2020 Feb 18.

Abstract

PURPOSE OF REVIEW

West Nile virus (WNV) emerged from Central Africa in the 1990s and is now endemic throughout much of the world. Twenty years after its introduction in the USA, it is becoming apparent that neurological impairments can persist for years following infection. Here, we review the epidemiological data in support of such long-term deficits and discuss possible mechanisms that drive these persistent manifestations.

RECENT FINDINGS

Focusing on the recently discovered antimicrobial roles of amyloid and alpha-synuclein, we connect WNV late pathology to overlapping features encountered in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. We also summarize new research on microglial activation and engulfment of neural synapses seen in recovered WNV as well as in neurodegenerative diseases, and discuss how loss of integrity of the blood-brain barrier (BBB) may exacerbate this process.

SUMMARY

Neuroinvasive viral infections such as WNV may be linked epidemiologically and mechanistically to neurodegeneration. This may open doors to therapeutic options for hitherto untreatable infectious sequelae; additionally, it may also shed light on the possible infectious etiologies of age-progressive neurodegenerative dementias.

摘要

综述目的

西尼罗河病毒(WNV)于20世纪90年代从中非出现,如今在世界大部分地区呈地方性流行。在美国引入该病毒20年后,越来越明显的是,感染后神经功能障碍可能会持续数年。在此,我们回顾支持此类长期缺陷的流行病学数据,并讨论导致这些持续表现的可能机制。

最新发现

聚焦于最近发现的淀粉样蛋白和α-突触核蛋白的抗菌作用,我们将西尼罗河病毒晚期病理与阿尔茨海默病和帕金森病等神经退行性疾病中遇到的重叠特征联系起来。我们还总结了关于康复的西尼罗河病毒感染者以及神经退行性疾病中所见的小胶质细胞活化和神经突触吞噬的新研究,并讨论血脑屏障(BBB)完整性丧失如何可能加剧这一过程。

总结

诸如西尼罗河病毒之类的神经侵袭性病毒感染可能在流行病学和机制上与神经退行性变相关。这可能为迄今无法治疗的感染后遗症打开治疗选择的大门;此外,它还可能揭示年龄相关性进行性神经退行性痴呆可能的感染病因。

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