Neurological injuries in COVID-19 patients: direct viral invasion or a bystander injury after infection of epithelial/en
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CLINICAL REVIEW
Neurological injuries in COVID-19 patients: direct viral invasion or a bystander injury after infection of epithelial/endothelial cells Sayed Ausim Azizi 1
&
Saara-Anne Azizi 2
Received: 29 June 2020 / Revised: 11 August 2020 / Accepted: 24 August 2020 # Journal of NeuroVirology, Inc. 2020
Abstract A subset of patients with coronavirus 2 disease (COVID-19) experience neurological complications. These complications include loss of sense of taste and smell, stroke, delirium, and neuromuscular signs and symptoms. The etiological agent of COVID-19 is SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), an RNA virus with a glycoprotein-studded viral envelope that uses ACE2 (angiotensin-converting enzyme 2) as a functional receptor for infecting the host cells. Thus, the interaction of the envelope spike proteins with ACE2 on host cells determines the tropism and virulence of SARS-CoV-2. Loss of sense of taste and smell is an initial symptom of COVID-19 because the virus enters the nasal and oral cavities first and the epithelial cells are the receptors for these senses. Stroke in COVID-19 patients is likely a consequence of coagulopathy and injury to cerebral vascular endothelial cells that cause thrombo-embolism and stroke. Delirium and encephalopathy in acute and post COVID-19 patients are likely multifactorial and secondary to hypoxia, metabolic abnormalities, and immunological abnormalities. Thus far, there is no clear evidence that coronaviruses cause inflammatory neuromuscular diseases via direct invasion of peripheral nerves or muscles or via molecular mimicry. It appears that most of neurologic complications in COVID-19 patients are indirect and as a result of a bystander injury to neurons. Keywords COVID-19 . Stroke . ACE2 . Taste . Smell . Encephalopathy . Tropism . SARS-CoV-2
In 2019, a new coronavirus disease (COVID-19) emerged, sparking a worldwide pandemic that has led to significant morbidity and mortality and stressed the health systems globally. Since the beginning of the pandemic, a deluge of unfiltered information has streamed into the scientific journals and mainstream media about COVID-19 and its etiological agent, SARS-CoV-2. This “infodemic” has often been in equal parts valuable, redundant, confusing, and contradictory. Although SARS-CoV-2 initially injures the respiratory tract, it also affects other organs including the nervous system (Helms et al. 2020a, b; Guan et al. 2020; Mao et al. 2020). Here, we review the salient features of SARS-CoV-2 pathogenesis and highlight the mechanisms of neurologic complications of the SARSCoV-2 infection. * Sayed Ausim Azizi [email protected] 1
Global Neuroscience Institute, 1 Medical Center Blvd., Chester, PA 19013, USA
2
Pritzker School of Medicine, University of Chicago, Chicago, USA
Human coronavirus 2 (SARS-CoV-2) The family of coronaviruses are a successful group of microbial pathogens that depend on the living cells for replication and infect many species of birds and mammals (Poutanen 2018). During the millions of y
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