Abstract
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. The olfactory dysfunction often occurs early in the course of the disease, and sometimes it is the only symptom in otherwise asymptomatic carriers. The cellular mechanisms for these specific olfactory disturbances in COVID-19 are now beginning to be elucidated. 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. 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. The emerging central role of sustentacular cells and inflammatory processes in the olfactory epithelium are particularly considered. 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. To answer this question, new systematic studies using an infectious virus and appropriate animal models are needed.
Highlights
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
The determination of the spatiotemporal expression pattern for ACE2 and TMPRSS2 allowed the formulation of a first consistent hypothesis explaining the mechanism leading to dysosmia in COVID-19
The current model of olfactory dysfunction in COVID-19 is based on the already proven observation that sustentacular cells (SUS) cells are the primary target of the virus and that SUSs infection initiates a series of events leading to dysosmia. This is a completely new look at virus-induced anosmia, since it has never been clearly shown for any other virus that the infection of SUS cells interferes with the perception of smell. Such a model of olfactory dysfunction in COVID-19 does not explicitly imply whether SARS-CoV-2 travels from the olfactory epithelium (OE) to the brain along olfactory axons
Summary
After the recognition of olfactory dysfunction as a COVID-19 symptom, it was proposed by Butowt and Bilinska[1] that non-neuronal cell-specific mechanism operating within the olfactory epithelium (OE) could play a major role. The latest work of Bryche and collaborators[5] using a hamster model showed the virus accumulation in SUS cells and not in ORNs. This study clearly indicates that very soon after infection specialized neuronal cilia containing olfactory receptors are lost, which is certainly synonymous with the loss of conduction of olfactory stimuli.[5] It seems, that even though there is a massive elimination of cells within the OE during the first days after infection, the sudden loss of smell is caused by an immediate damage to the cilia structure.[5] It is accepted that the perception of smell is restored in most patients within 1−2 weeks. Lack of information on which patients experienced anosmia makes it difficult to interpret these results unambiguously
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