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隐匿的入侵者:揭开嗜神经病毒之谜及其在脑脊液中难以捉摸的存在——一篇综述

Stealth invaders: unraveling the mystery of neurotropic viruses and their elusive presence in cerebrospinal fluid - a comprehensive review.

作者信息

Srichawla Bahadar S, Kipkorir Vincent, Manan Muhammad Romail, Dhali Arkadeep, Diebel Sebastian, Sawant Tirtha, Zia Subtain, Carrion-Alvarez Diego, Suteja Richard C, Nurani Khulud, Găman Mihnea-Alexandru

机构信息

Department of Neurology.

Department of Human Anatomy and Physiology, University of Nairobi, University Way, Nairobi, Kenya.

出版信息

Ann Med Surg (Lond). 2023 Apr 27;85(6):2761-2766. doi: 10.1097/MS9.0000000000000736. eCollection 2023 Jun.

DOI:10.1097/MS9.0000000000000736
PMID:37363567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10289609/
Abstract

Neurotropic viruses are a threat to human populations due to ongoing zoonosis. A wide array of neurological manifestations can occur most often including parkinsonism, encephalitis/encephalopathy, flaccid myelitis, and Guillain-Barré syndrome. Neuroinvasion occurs through: transneural transmission, blood brain barrier (BBB) dysfunction, and 'trojan horse' mechanism or infected immune cell trafficking into the central nervous system (CNS). Transneural transmission occurs through virus mediated hijacking of intracellular transport proteins allowing retrograde viral transport. BBB dysfunction occurs through cytokine storm increasing membrane permissibility. Increased chemokine expression allows leukocyte trafficking to the BBB. Virally infected leukocytes may successfully pass through the BBB allowing the pathogen to infect microglia and other CNS cell types. We define cerebrospinal fluid (CSF) nondetection as a virus' ability to evade direct CSF detection but still causing significant neurological symptoms and disease. Mechanisms of CSF nondetection include: transneuronal propagation through trans-synaptic transmission, and synaptic microfusion, as well as intrathecal antibody synthesis and virus neutralization. Direct virus detection in CSF is associated with an increased neurological disease burden. However, the lack of CSF detection does not exclude CNS involvement due to possible neuroevasive mechanisms.

摘要

由于持续存在的人畜共患病,嗜神经病毒对人类构成威胁。最常出现的一系列神经学表现包括帕金森症、脑炎/脑病、弛缓性脊髓炎和格林-巴利综合征。神经侵袭通过以下方式发生:经神经传播、血脑屏障(BBB)功能障碍以及“特洛伊木马”机制或受感染免疫细胞向中枢神经系统(CNS)的转运。经神经传播是通过病毒介导劫持细胞内转运蛋白实现逆行病毒转运。血脑屏障功能障碍是通过细胞因子风暴增加膜通透性而发生的。趋化因子表达增加使白细胞向血脑屏障转运。病毒感染的白细胞可能成功穿过血脑屏障,使病原体感染小胶质细胞和其他中枢神经系统细胞类型。我们将脑脊液(CSF)未检测到定义为病毒逃避直接脑脊液检测但仍引起明显神经症状和疾病的能力。脑脊液未检测到的机制包括:通过跨突触传递和突触微融合进行跨神经元传播,以及鞘内抗体合成和病毒中和。脑脊液中直接检测到病毒与神经疾病负担增加有关。然而,由于可能存在神经逃避机制,脑脊液检测不到并不排除中枢神经系统受累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/41332242f1a9/ms9-85-2761-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/6cea4b73cffb/ms9-85-2761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/bba15e4e8857/ms9-85-2761-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/41332242f1a9/ms9-85-2761-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/6cea4b73cffb/ms9-85-2761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/bba15e4e8857/ms9-85-2761-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95a/10289609/41332242f1a9/ms9-85-2761-g003.jpg

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