SARS-CoV-2 neurotropism and other possible causes of olfactory disorders in COVID-19

Abstract

Coronavirus disease 2019 (COVID-19) is an acute infectious respiratory disease (AIRD) caused by infection with the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first cases were diagnosed and reported in Wuhan, central China, in November 2019. The disease initially occurred locally. However, the number of infected individuals increased dynamically and spread worldwide. The most common symptoms of the SARS-CoV-2 infection include malaise, fever, dry cough and dyspnoea. Over time, reports of new COVID-19 symptoms included taste and smell disorders. A potential cause of these disorders is related to neurotropism, i.e. the affinity of SARS-CoV-2 to the nervous system. Angiotensin-converting enzyme 2 receptor is essential in the pathogenesis of SARS-CoV-2 infection. The receptor is found in many tissues and organs, including the olfactory epithelium, neurons and neuroglial cells. Another potential cause is neuroinvasiveness, i.e. the ability of the virus to invade the central nervous system, and thereby damage its structures. As a result, olfactory disorders may occur. Other concepts, such as the inflammatory response of the body and the concept of stroke or damage to olfactory supporting cells, are also considered.

SARS-CoV-2 and the nervous system

“…It is assumed that in such cases the cause of anosmia/hyposmia is the depletion of sustentacular cells caused by the SARS-CoV-2 infection and their subsequent restoration by days 10-14 post-infection. However, in some patients, the sense of smell is permanently damaged [18]. This is quite difficult to explain because olfactory sensory neurons do not express a receptor protein for SARS-CoV-2, and are not infected or destroyed by this virus.…”