Abstract
The irruption of SARS-CoV-2 during 2020 has been of pandemic proportions due to its rapid spread and virulence. COVID-19 patients experience respiratory, digestive and neurological symptoms. Distinctive symptom as anosmia, suggests a potential neurotropism of this virus. Amongst the several pathways of entry to the nervous system, we propose an alternative pathway from the infection of the gut, involving Toll-like receptor 4 (TLR4), zonulin, protease-activated receptor 2 (PAR2) and zonulin brain receptor. Possible use of zonulin antagonists could be investigated to attenuate neurological manifestations caused by SARS-CoV-19 infection.
Highlights
SARS-CoV-2 emerged in December 2019 and rapidly caused a global pandemic extending along 2020
We found that neurological and gastrointestinal symptoms were frequent in hospitalized patients: 54.5% and 53.2%, respectively
The aim of the present review is to develop a feasible hypothesis complementary to the current information that exists regarding the SARS-CoV-2 virus’ journey to the brain [9]
Summary
SARS-CoV-2 emerged in December 2019 and rapidly caused a global pandemic extending along 2020. This suggests that the hematogenous route is the most likely route for SARSCoV-2 to the brain Considering all this data together and in line with our results (Table 1), we propose that the increased intestinal permeability caused by overexpression of zonulin opens an entry door for SARS‐CoV‐2. Through this way, the virus reaches the bloodstream or the lymphatic system, infects endothelial cells of blood or lymphatic vessels, infects local tissues, and is disseminated to many organs, including the CNS. The spike protein binds TLR4 and, via MyD88, induces the expression of proinflammatory cytokines, especially IL-6 This cytokine promotes the overexpression of zonulin, which, via PAR2, disassembles TJ, opening paracellular pathways and allowing the virus to pass through. We hope that this article will open up the possibility of investigating the effect of zonulin antagonists on the attenuation of neurological symptoms caused by SARS-CoV-19 infection
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