Neurology Department, Astrakhan State Medical University, Astrakhan, Russia.
Center for Developmental Neuroscience, City University of New York, College of Staten Island, New York, USA.
Neurol Sci. 2020 Oct;41(10):2657-2669. doi: 10.1007/s10072-020-04575-3. Epub 2020 Jul 28.
Respiratory viruses are opportunistic pathogens that infect the upper respiratory tract in humans and cause severe illnesses, especially in vulnerable populations. Some viruses have neuroinvasive properties and activate the immune response in the brain. These immune events may be neuroprotective or they may cause long-term damage similar to what is seen in some neurodegenerative diseases. The new "Severe Acute Respiratory Syndrome Coronavirus 2" (SARS-CoV-2) is one of the Respiratory viruses causing highly acute lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical similarities to those reported in "Severe Acute Respiratory Syndrome Coronavirus"(SARS-CoV) and the "Middle East Respiratory Syndrome Coronavirus"(MERS-CoV) including neurological manifestation. To examine the possible neurological damage induced by SARS-CoV-2, it is necessary to understand the immune reactions to viral infection in the brain, and their short- and long-term consequences. Considering the similarities between SARS-CoV and SARS-CoV-2, which will be discussed, cooperative homological and phylogenetical studies lead us to question if SARS-CoV-2 can have similar neuroinvasive capacities and neuroinflammatiory events that may lead to the same short- and long-term neuropathologies that SARS-CoV had shown in human and animal models. To explain the neurological manifestation caused by SARS-CoV-2, we will present a literature review of 765 COVID-19 patients, in which 18% had neurological symptoms and complications, including encephalopathy, encephalitis and cerebrovascular pathologies, acute myelitis, and Guillain-Barré syndrome. Clinical studies describe anosmia or partial loss of the sense of smell as the most frequent symptom in COVID19 patients, suggesting that olfactory dysfunction and the initial ultrarapid immune responses could be a prognostic factor.
呼吸道病毒是机会性病原体，可感染人类上呼吸道并导致严重疾病，尤其是在弱势群体中。一些病毒具有神经侵袭性，并在大脑中激活免疫反应。这些免疫事件可能具有神经保护作用，也可能导致类似于某些神经退行性疾病所见的长期损害。新的“严重急性呼吸系统综合征冠状病毒 2 型”（SARS-CoV-2）是引起高度急性致死性肺炎冠状病毒病 2019（COVID-19）的呼吸道病毒之一，其临床特征与“严重急性呼吸系统综合征冠状病毒”（SARS-CoV）和“中东呼吸系统综合征冠状病毒”（MERS-CoV）报告的相似，包括神经系统表现。为了研究 SARS-CoV-2 可能引起的神经损伤，有必要了解病毒感染大脑中的免疫反应及其短期和长期后果。考虑到 SARS-CoV 和 SARS-CoV-2 之间的相似性，我们将讨论合作同源性和系统发育研究，我们不禁要问 SARS-CoV-2 是否具有类似的神经侵袭能力和神经炎症事件，这些事件可能导致 SARS-CoV 在人类和动物模型中表现出相同的短期和长期神经病理学。为了解释 SARS-CoV-2 引起的神经系统表现，我们将对 765 名 COVID-19 患者的文献进行综述，其中 18%的患者出现神经系统症状和并发症，包括脑病、脑炎和脑血管疾病、急性脊髓炎和格林-巴利综合征。临床研究描述了 COVID19 患者中最常见的嗅觉障碍或嗅觉部分丧失症状，表明嗅觉功能障碍和最初的超快速免疫反应可能是一个预后因素。
