Tavčar Petra, Potokar Maja, Kolenc Marko, Korva Miša, Avšič-Županc Tatjana, Zorec Robert, Jorgačevski Jernej
Laboratory of Neuroendocrinology-Molecular Cell Physiology, Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Celica Biomedical, Ljubljana, Slovenia.
Front Cell Neurosci. 2021 Apr 9;15:662578. doi: 10.3389/fncel.2021.662578. eCollection 2021.
At the end of 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was discovered in China, causing a new coronavirus disease, termed COVID-19 by the WHO on February 11, 2020. At the time of this paper (January 31, 2021), more than 100 million cases have been recorded, which have claimed over 2 million lives worldwide. The most important clinical presentation of COVID-19 is severe pneumonia; however, many patients present various neurological symptoms, ranging from loss of olfaction, nausea, dizziness, and headache to encephalopathy and stroke, with a high prevalence of inflammatory central nervous system (CNS) syndromes. SARS-CoV-2 may also target the respiratory center in the brainstem and cause silent hypoxemia. However, the neurotropic mechanism(s) by which SARS-CoV-2 affects the CNS remain(s) unclear. In this paper, we first address the involvement of astrocytes in COVID-19 and then elucidate the present knowledge on SARS-CoV-2 as a neurotropic virus as well as several other neurotropic flaviviruses (with a particular emphasis on the West Nile virus, tick-borne encephalitis virus, and Zika virus) to highlight the neurotropic mechanisms that target astroglial cells in the CNS. These key homeostasis-providing cells in the CNS exhibit many functions that act as a favorable milieu for virus replication and possibly a favorable environment for SARS-CoV-2 as well. The role of astrocytes in COVID-19 pathology, related to aging and neurodegenerative disorders, and environmental factors, is discussed. Understanding these mechanisms is key to better understanding the pathophysiology of COVID-19 and for developing new strategies to mitigate the neurotropic manifestations of COVID-19.
2019年底，在中国发现了严重急性呼吸综合征冠状病毒2（SARS-CoV-2），引发了一种新型冠状病毒疾病，世界卫生组织于2020年2月11日将其命名为COVID-19。在撰写本文时（2021年1月31日），全球已记录了超过1亿例病例，死亡人数超过200万。COVID-19最重要的临床表现是重症肺炎；然而，许多患者出现各种神经症状，从嗅觉丧失、恶心、头晕、头痛到脑病和中风，炎症性中枢神经系统（CNS）综合征的患病率很高。SARS-CoV-2也可能靶向脑干中的呼吸中枢并导致无症状性低氧血症。然而，SARS-CoV-2影响中枢神经系统的嗜神经机制仍不清楚。在本文中，我们首先探讨星形胶质细胞在COVID-19中的作用，然后阐明目前关于SARS-CoV-2作为嗜神经病毒以及其他几种嗜神经黄病毒（特别强调西尼罗河病毒、蜱传脑炎病毒和寨卡病毒）的知识，以突出靶向中枢神经系统星形胶质细胞的嗜神经机制。中枢神经系统中这些提供关键内环境稳定的细胞具有许多功能，这些功能为病毒复制提供了有利环境，对SARS-CoV-2来说可能也是如此。本文还讨论了星形胶质细胞在与衰老、神经退行性疾病和环境因素相关的COVID-19病理学中的作用。了解这些机制是更好地理解COVID-19病理生理学以及制定减轻COVID-19嗜神经表现的新策略的关键。
