SARS-CoV-2, an Underestimated Pathogen of the Nervous System
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COVID-19
SARS-CoV-2, an Underestimated Pathogen of the Nervous System Shweta Jakhmola 1 & Omkar Indari 1 & Sayantani Chatterjee 1 & Hem Chandra Jha 1 Accepted: 10 September 2020 # Springer Nature Switzerland AG 2020
Abstract Numerous clinical studies have reported neurological symptoms in COVID-19 patients since the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), apart from the atypical signs of pneumonia. Angiotensin-converting enzyme-2 (ACE-2), a potential receptor for SARS-CoV-2 entry, is expressed on various brain cells and cerebral parts, i.e., subfornical organ, paraventricular nucleus, nucleus of the tractus solitarius, and rostral ventrolateral medulla, as well as in non-cardiovascular areas such as the motor cortex and raphe. The resident CNS cells like astrocytes and microglia also express ACE-2, thus highlighting the vulnerability of the nervous system to SARS-CoV-2 infection. Additionally, transmembrane serine protease 2 (TMPRSS2) and furin facilitate virus entry into the host. Besides, the probable routes of virus entry into the nervous system include the hematogenic pathway, through the vagus, the olfactory nerve, or the enteric nervous system. However, the trajectory of SARS-CoV-2 to the brain needs investigation. Furthermore, a Th17-mediated cytokine storm is seen in COVID-19 cases with higher levels of IL-1β/2/7/8/9/ 10/17, GM-CSF, IFN-γ, TNF-α, CXCL-10, MCP1, and MIP1α/β. Some cytokines can cross the blood-brain barrier and activate the brain’s immune cells to produce neural cytokines, leading to neuronal dysfunctions. Nonetheless, most of the neurological conditions developed due to viral infections may not have effective and registered treatments. Although, some antivirals may inhibit the virus-mediated pathogenesis and prove to be suitable in COVID-19 treatment. Therefore, clinicians’ and researchers’ collective expertise may unravel the potential of SARS-CoV-2 infection to prevent short-term and long-term CNS damage. Keywords SARS-CoV-2 . COVID-19 . ACE-2 . Nervous system . Cytokine storm
Introduction The initial cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection appeared in December 2019 in Hubei province, China [1]. Since then, it has become a global threat. Besides systemic and respiratory ailments, 36.4% of coronavirus disease of 2019 (COVID-19) patients developed neurological symptoms [2]. Additionally, taste, smell, and visual impairments are reported in several cases of COVID-19 [2]. SARS-CoV-2, a human CoV (HCoV) belongs to β-coronaviruses, and various clinical and pre-clinical studies have reported potential neurovirulent properties of these viruses [3]. Furthermore, the presence of
This article is part of the topical collection on Covid-19 * Hem Chandra Jha [email protected] 1
Infection Bio-engineering Group, Discipline of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Lab No. 302, School Building, Indore, Madhya Pradesh 453552, India
SARS-CoV-2 in cerebrospinal fluid (CSF) of COVID-19 patient
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