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COVID-19 may target CNS, anosmia and dysgeusia suggest

Natalia Reoutova
07 Apr 2020

Loss of the senses of smell and taste reported in patients suggests that coronavirus disease 2019 (COVID-19) may affect the central nervous system (CNS). Tissue distribution of angiotensin-converting enzyme 2 (ACE2) receptor used by the virus to enter human cells hints at the possible contribution of neurological tissue damage to the morbidity and mortality caused by COVID-19.

Recent reports suggest an association between COVID-19 and altered olfactory function. [Rhinology 2020, doi: 10.4193/Rhin20.114] ENT UK (Ear, Nose and Throat UK), the British Association of Otorhinolaryngology, reported in a guidance document that significant numbers of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in China, France, Germany (>66 percent), Iran, Northern Italy, South Korea (30 percent), and the US developed anosmia or hyposmia. [https://www.entuk.org/sites/default/files/files/Loss%20of%20sense%20of%20smell%20as%20marker%20of%20COVID.pdf]

In view of the rapidly accumulating anecdotal evidence that anosmia with resultant dysgeusia are frequently reported symptoms associated with COVID-19, the American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) has established the COVID-19 Anosmia Reporting Tool for Clinicians on 26 March 2020. [https://www.entnet.org/content/reporting-tool-patients-anosmia-related-covid-19]

A review article from Jilin University in China suggests that SARS-CoV-2 may target neurons in the medulla oblongata, contributing to acute respiratory failure. “The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most patients admitted to intensive care units are unable to breathe spontaneously. Additionally, some patients with COVID‐19 show neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the CNS, inducing neurological diseases,” wrote the authors. [J Med Virol 2020, doi: 10.1002/jmv.25728; medRxiv 2020, doi: 10.1101/2020.02.22.20026500]

SARS‐CoV has been identified in the brains of patients, and previous studies have shown its ability to cause neuronal death in mice by invading the brain via the nose close to the olfactory epithelium. [J Virol 2008;82:7264-7275] Furthermore, some coronaviruses have demonstrated the ability to spread via a synapse‐connected route to the medullary cardiorespiratory centre from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Given the high degree of homology between COVID-19 and SARS‐CoV, the potential CNS invasion by the former may be partially responsible for the acute respiratory failure.

Same as SARS-CoV, SARS-CoV-2exploits the ACE2 receptor by using spike protein S1 to gain cell entry. The binding affinity of SARS-CoV-2’s S1 ectodomain is 10-fold to 20-fold higher than that of SARS-CoV. [Science 2020;367:1260-1263] ACE2 receptors are expressed on the surfaces of glial cells and neurons, making them a potential infection target. [Database (Oxford) 2018, doi: 10.1093/database/bay003]

“Movement of the COVID-19 virus to the brain via the cribriform plate close to the olfactory bulb can be an additional pathway that could enable the virus to reach and affect the brain. Findings like an altered sense of smell or hyposmia in an uncomplicated early-stage COVID-19 patient should be investigated thoroughly for CNS involvement,” suggested researchers from the Aga Khan University in Pakistan. [ACS Chem Neurosci 2020;11:995-998]

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