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Understanding the neurotropic characteristics of SARS-CoV-2: from neurological manifestations of COVID-19 to potential neurotropic mechanisms.
Journal of Neurology ( IF 4.8 ) Pub Date : 2020-05-26 , DOI: 10.1007/s00415-020-09929-7
Zhiqiang Zhou 1 , Huicong Kang 2 , Shiyong Li 1 , Xu Zhao 3
Affiliation  

Coronavirus disease 2019 (COVID-19), a disease caused by the novel betacoronavirus (SARS-CoV-2), has become a global pandemic threat. The potential involvement of COVID-19 in central nervous system (CNS) has attracted considerable attention due to neurological manifestations presented throughout the disease process. In addition, SARS-CoV-2 is structurally similar to SARS-CoV, and both bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. Thus, cells expressing ACE2, such as neurons and glial cells may act as targets and are thus vulnerable to SARS-CoV-2 infection. Here, we have reviewed the neurological characteristics of COVID-19 and summarized possible mechanisms of SARS-CoV-2 invasion of the CNS. COVID-19 patients have presented with a number of different neurological symptoms such as headache, dizziness, hyposmia, and hypogeusia during the course of illness. It has also been reported recently that some cases of COVID-19 have presented with concurrent acute cerebrovascular disease (acute ischemic stroke, cerebral venous sinus thrombosis, cerebral hemorrhage, subarachnoid hemorrhage), meningitis/encephalitis, acute necrotizing hemorrhagic encephalopathy, and acute Guillain–Barré syndrome. Furthermore, SARS-CoV-2 RNA detected in a cerebrospinal fluid specimen of a patient with COVID-19 have provided direct evidence to support the theory of neurotropic involvement of SARS-CoV-2. However, the underlying neurotropic mechanisms of SARS-CoV-2 are yet to be established. SARS-CoV-2 may affect CNS through two direct mechanisms (hematogenous dissemination or neuronal retrograde dissemination) or via indirect routes. The underlying mechanisms require further elucidation in the future.



中文翻译:

了解 SARS-CoV-2 的嗜神经特征:从 COVID-19 的神经学表现到潜在的嗜神经机制。

2019 年冠状病毒病 (COVID-19) 是一种由新型 β 冠状病毒 (SARS-CoV-2) 引起的疾病,已成为全球流行病威胁。由于在整个疾病过程中出现的神经系统表现,COVID-19 在中枢神经系统 (CNS) 中的潜在参与引起了相当大的关注。此外,SARS-CoV-2在结构上与SARS-CoV相似,都与血管紧张素转换酶2(ACE2)受体结合进入人体细胞。因此,表达 ACE2 的细胞(例如神经元和神经胶质细胞)可以作为靶标,因此容易受到 SARS-CoV-2 感染。在这里,我们回顾了 COVID-19 的神经学特征,并总结了 SARS-CoV-2 侵入中枢神经系统的可能机制。COVID-19 患者出现了许多不同的神经系统症状,如头痛、头晕、嗅觉减退、和病程中的味觉减退。最近也有报道称,部分 COVID-19 病例并发急性脑血管疾病(急性缺血性中风、脑静脉窦血栓形成、脑出血、蛛网膜下腔出血)、脑膜炎/脑炎、急性坏死性出血性脑病和急性格林-巴雷综合征。此外,在一名 COVID-19 患者的脑脊液样本中检测到的 SARS-CoV-2 RNA 为支持 SARS-CoV-2 的嗜神经参与理论提供了直接证据。然而,SARS-CoV-2 的潜在嗜神经机制尚未确定。SARS-CoV-2 可能通过两种直接机制(血行传播或神经元逆行传播)或间接途径影响中枢神经系统。

更新日期:2020-05-26
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