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. 2021 Jun 7;18:120. doi: 10.1186/s12985-021-01578-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — SARS-CoV-2 causes damage to the nervous system via 4 possible pathways: (1) direct viral encephalitis which caused by direct damage to brain tissue by SARs-CoV-2 as it enters brain cells through ACE2 receptors and causes inflammation and damage. The S (spike) proteins that cover the surface of the virus bind to ACE2 receptors and facilitate viral entry. Once the S protein binds to ACE2 receptor, TM protease serine 2 (TMPRSS2) located in the host cell membrane further facilitates virus entry by activating the S protein. After the virus has entered the host cell, viral RNA is released and protein cleavage and assembly of replicase-transcriptase lead to transcription and replication of viral genome [39]. (2) Systemic inflammation: SARS-CoV-2 infection elicits cytokine storm in the body which, along with severe sepsis can lead to Hippocampal atrophy. (3) cerebrovascular changes: the viral protein ORF3 and ventilation induced hypoxia activate inflammasome NLRP3 which can lead to increase in inflammatory cytokines especially IL-19 IL-1B which can trigger the inflammatory cascade causing impairment of immune system of the brain leading to deposition of pathological fibrillary tangles in brain tissue, and impatient of cerebral hemostasis and function[40]. (4) peripheral organ damage due to systemic inflammation and direct viral infection via ACE2 receptors and ARDS can lead to long term cognitive decline [36] (Image created with BioRender.com)