ABSTRACT
OBJECTIVE: The novel coronavirus disease-19 (COVID-19) pandemic had intense social and economic effects. Patients infected with COVID-19 may present with a series of conditions. A considerable number of patients express taste and smell disturbances as a prodromal, coexistent, or as the only manifestation of COVID-19 infection. The objective of the present review is to review the hypothetical mechanisms of action and etiopathogenesis of dysgeusia in COVID-19 patients. MATERIALS AND METHODS: Multiple scientific databases were explored, including PubMed, Medline, Scopus, Cochrane-library, LILACS, Livivo and OpenGrey. All types of articles that discussed the pathogenesis of dysgeusia were included, while articles that described dysgeusia without detail about its mode of action were excluded. RESULTS: A total of 47 articles, with different designs, were included in this review. These articles suggested direct viral neural invasion to olfactory and gustatory nerves, viral cytotoxicity to taste buds, angiotensin II imbalance, augmented pro-inflammatory cytokines, and disturbances in salivary glands and sialic acid. COVID-19 induced-dysgeusia was also associated with systemic diseases, medications, zinc, chemicals, and disinfectants. CONCLUSIONS: The most likely cause of transient dysgeusia in COVID-19 is peripheral neurotropism and direct toxicity to taste buds or olfactory epithelium. Other factors may also play a contributory role in dysgeusia, such as a defect in the quality and quantity of saliva, pro-inflammatory cytokines, angiotensin II accumulation, systemic diseases, hypozincemia, and excessive use of chemicals.
Subject(s)
COVID-19/complications , COVID-19/metabolism , Dysgeusia/etiology , Dysgeusia/metabolism , Ageusia/diagnosis , Ageusia/etiology , Ageusia/metabolism , COVID-19/diagnosis , Dysgeusia/diagnosis , Humans , Olfaction Disorders/diagnosis , Olfaction Disorders/etiology , Olfaction Disorders/metabolism , Prospective Studies , Renin-Angiotensin System/physiology , Retrospective Studies , Smell/physiology , Taste/physiologySubject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/complications , Coronavirus Infections/metabolism , Olfaction Disorders/etiology , Olfactory Mucosa/metabolism , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/complications , Pneumonia, Viral/metabolism , Angiotensin-Converting Enzyme 2 , COVID-19 , Humans , Olfaction Disorders/metabolism , Pandemics , SARS-CoV-2 , Virus ReplicationSubject(s)
Coronavirus Infections/physiopathology , Dysgeusia/physiopathology , Olfaction Disorders/physiopathology , Pneumonia, Viral/physiopathology , Angiotensin-Converting Enzyme 2 , Betacoronavirus/metabolism , COVID-19 , Coronavirus Infections/complications , Dysgeusia/etiology , Dysgeusia/metabolism , Humans , Mouth Mucosa/metabolism , Olfaction Disorders/etiology , Olfaction Disorders/metabolism , Olfactory Mucosa/metabolism , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/complications , SARS-CoV-2ABSTRACT
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.
Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Olfaction Disorders/etiology , Olfaction Disorders/virology , Olfactory Receptor Neurons/cytology , Olfactory Receptor Neurons/virology , Pneumonia, Viral/complications , Animals , COVID-19 , Coronavirus Infections/metabolism , Humans , Olfaction Disorders/metabolism , Olfactory Receptor Neurons/metabolism , Pandemics , Pneumonia, Viral/metabolism , SARS-CoV-2 , Smell/physiologyABSTRACT
Studies have found increased rates of dysosmia in patients with Novel Coronavirus disease 2019 (COVID-19). However, the mechanism that causes olfactory loss is unknown. The primary objective of this study was to explore local proinflammatory cytokine levels in the olfactory epithelium in patients with COVID-19. Biopsies of the olfactory epithelium were taken from patients with confirmed COVID-19 as well as uninfected controls. Levels of tumor necrosis factor α (TNF-α) and interleukin-1-beta (IL-1ß) were assessed using ELISA and compared between groups. Average TNF-α levels were significantly increased in the olfactory epithelium of the COVID-19 group compared to the control group (P < 0.05). However, no differences in IL-1ß were seen between groups. Elevated levels of the proinflammatory cytokine TNF-α were seen in the olfactory epithelium in patients with COVID-19. This suggests that direct inflammation of the olfactory epithelium could play a role in the acute olfactory loss described in many patients with COVID-19.