• Antônio Kleiton de Sousa, Magalhães Diva de Aguiar DA Laboratory of Experimental Physiopharmacology (LAFFEX), Federal University of the Delta of Parnaíba, Parnaíba, PI, Brazil; The Northeast Biote, Jayro Dos Santos Ferreira, and André Luiz Dos Reis Barbosa.
• Laboratory of Experimental Physiopharmacology (LAFFEX), Federal University of the Delta of Parnaíba, Parnaíba, PI, Brazil.
• Med. Hypotheses. 2020 Nov 1; 144: 110213.

AbstractAt the end of 2019, there was an outbreak of a new Coronavirus 2019 (COVID-19 disease). Studies suggest that SARS-CoV-2 can cause infection in the central nervous system (CNS) and trigger neurological symptoms that include headache, nausea and vomiting, mental confusion and loss of smell or taste. These findings reveal that Coronaviruses have neurological tropism and neuroinvasive capacity. The spread of SARS-CoV-2 in the brain tissue possibly occurs through the systemic circulation as reported in patients affected by SARS-CoV. Evidence highlights similarity between the SARS-CoV genome and SARS-CoV-2 and that both interact with the angiotensin-converting enzyme type 2 (ACE2) located in the brain tissue of infected patients. Hence, the presence of ACE2 is likely in the CNS to mediate the entry of the SARS-CoV-2 virus into neural tissue. Our hypothesis suggests that SARS-CoV-2 can cause encephalitis through the production of inflammatory mediators and activation of immune system cells resulting from the interaction of the ACE2 receptor with the viral Spike protein that causes an increase in angiotensin II. This mechanism has the ability to activate immune system cells by exacerbating stimuli at the angiotensin 2 receptor (AT2R). Thus, it leads to a status of brain injury preceded by vascular damage and destruction of the blood-brain barrier, making it responsible for the installation of acute inflammation.Copyright © 2020 Elsevier Ltd. All rights reserved.

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