![]() The high incidence of olfactory dysfunction in COVID-19 and its possible implications on the brain have directed part of current research on COVID-19 toward a thorough understanding of this process at the mechanistic level. It is a bit surprising, however, that although anosmia is often linked with many human viruses causing common cold (e.g., influenza and coronaviruses), its exact cellular and molecular mechanism has not yet been clearly established. ![]() Finally, most obvious cause of COVID-19-associated anosmia may be direct damage to olfactory receptor neurons (ORNs), as other human coronaviruses (e.g., OC43) were previously shown to directly bind to ORNs. Thus, excessive and systemic inflammatory response in the brain unlikely plays a causative role in the developing anosmia. Moreover, there is no solid data supporting the rapid damage to olfactory cortical areas in the brain, considering that anosmia is often detected very early on in the disease both in mild cases and even asymptomatic patients. On the other hand, rhinorrhea or associated nasal obstruction which could block nasal air flow is known to be much less often observed in COVID-19 as compared to the frequency of olfactory deficits. Olfactory cleft syndrome has been reported solely in rare cases. Initial hospital observations and early studies have suggested several possible mechanisms for the development of anosmia in COVID-19, including olfactory cleft syndrome, nasal obstruction and rhinorrhea, cytokine storm, direct damage to olfactory receptor neurons (ORNs), and impairment of the olfactory perception centers in the brain. To answer this question, new systematic studies using an infectious virus and appropriate animal models are needed. The proposed model of anosmia in COVID-19 does not answer unequivocally whether the new coronavirus exploits the olfactory route to rapidly or slowly reach the brain in COVID-19 patients. The emerging central role of sustentacular cells and inflammatory processes in the olfactory epithelium are particularly considered. In this Viewpoint, we discuss current progress in research on olfactory dysfunction in COVID-19 and we also propose an updated model of the SARS-CoV-2-induced dysosmia. ![]() Several very recent papers contributed to explaining the key cellular steps occurring in the olfactory epithelium leading to anosmia/hyposmia (collectively known as dysosmia) initiated by SARS-CoV-2 infection. The cellular mechanisms for these specific olfactory disturbances in COVID-19 are now beginning to be elucidated. The olfactory dysfunction often occurs early in the course of the disease, and sometimes it is the only symptom in otherwise asymptomatic carriers. It has become clear since the pandemic broke out that SARS-CoV-2 virus causes reduction of smell and taste in a significant fraction of COVID-19 patients.
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