Abstract
The recent pandemic of coronavirus infectious illness 2019 (COVID19) triggered by SARS-CoV-2 has rapidly spread around the globe, generating in severe events an acute, highly lethal pneumonia and death. In the past two hitherto similar CoVs, the severe acute respiratory syndrome CoV (SARS-CoV-1) and Middle East respiratory syndrome CoV (MERS-CoV) also gained universal attention as they produced clinical symptoms similar to those of SARS-CoV-2 utilizing angiotensin-converting enzyme 2 (ACE2) receptor and dipeptidyl peptidase 4 (DPP4) to go into the cells. COVID-19 may also present with overtly neurological symptoms. The proper understanding of the expression and dissemination of ACE2 in central and peripheral nerve systems is crucial to understand better the neurological morbidity caused by COVID-19. Using the STRING bioinformatic tool and references through text mining tools associated to Coronaviruses, we identified SAMHD1 as the probable link to neurological symptoms. Paralleled to the response to influenza A virus and, specifically, respiratory syncytial virus, SARS-CoV-2 evokes a response that needs robust induction of a subclass of cytokines, including the Type I and, obviously, Type III interferons as well as a few chemokines. We correlate ACE2 to the pathogenesis and neurologic complications of COVID-19 and found that SAMHD1 links to NF-κB pathway. No correlation was found with other molecules associated with Coronavirus infection, including ADAR, BST2, IRF3, IFITM3, ISG15, MX1, MX2, RNASEL, RSAD2, and VPRBP. We suggest that SAMHD1 is the molecule that may be behind the mechanisms of the neurological complications associated with COVID-19.
Highlights
Coronaviruses (CoVs), which belong to Coronaviridae family, are enveloped RNA viruses that have been associated with respiratory and extra-respiratory diseases in various animal species [1]
Taken together, based on its similarity with other CoVs, and the fact that COVID 29 is neuroinvasive and its functional receptor is angiotensin-converting enzyme 2 (ACE2), and because SAMDH1 is upregulated in the pathogenesis of COVID 19, it can be hypothesized that the SARS-CoV-2 entry into the brain will result in long-term neurological sequelae and may lead to neurodegenerative changes
We discussed the distribution of ACE2 in central nervous system (CNS) and its vital role regulation of cardiovascular function and, blood pressure in the brain and at the periphery
Summary
Coronaviruses (CoVs), which belong to Coronaviridae family, are enveloped RNA viruses that have been associated with respiratory and extra-respiratory (e.g., enteric and neurological) diseases in various animal species [1]. Pondering the high similarity between SARS-CoV-1 and SARS-CoV-2, some preliminary studies are suggesting that the potential CNS invasion may partially be responsible for the mortality (other than morbidity) associated with COVID-19 infection and have some late neurologic sequelae [8, 11]. These enveloped viruses harbor a positive-strand RNA genome with dimensions of up to 31 kb, which is representative of the largest known genome including all RNA viruses [9].
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