ABSTRACT
Background: Bitter taste-sensing type 2 receptor (T2Rs or TAS2Rs) found on ciliated epithelial cells and solitary chemosensory cells have a role in respiratory tract immuni-ty. T2Rs have shown protection against SARS-CoV-2 by enhancing the innate immune response. The purpose of this review is to outline the current sphere of knowledge re-garding this association. Method(s): A narrative review of the literature was done by searching (T2R38 OR bitter taste receptor) AND (COVID-19 OR SARS-CoV-2) keywords in PubMed and google scholar. Result(s): T2R38, an isoform of T2Rs encoded by the TAS2R38 gene, may have a potential association between phenotypic expression of T2R38 and prognosis of COVID-19. Current studies suggest that due to different genotypes and widespread distributions of T2Rs within the respiratory tract and their role in innate immunity, treatment protocols for COVID-19 and other respiratory diseases may change accordingly. Based on the phenotypic expression of T2R38, it varies in innate immunity and host response to respiratory infection, systemic symptoms and hospitalization. Conclusion(s): This review reveals that patients' innate immune response to SARS-COV-2 could be influenced by T2R38 receptor allelic variations.Copyright © 2023, Avicenna Journal of Medical Biotechnology.
ABSTRACT
COVID19 is characterized by alteration of smell and taste perception. It was investigated the presence of alteration for cold, heat, and food consistency perception in COVID-19 patients and the possible correlation with the most commonly used biomarkers in a routine way (CRP, IL-6, IL-1, PSP, PCT) to show if the local inflammatory process may induce alteration of cold, heat, and food consistency perception in COVID-19. From March 2020 to April 2021, a survey about taste and oral tactile/thermal sensitivity dysfunction was carried out on 1155 patients with mild or moderate COVID-19, while patients admitted to intensive care were excluded because they could not answer questions from health professionals. Positive RT-PCR confirmed all diagnoses. CRP, IL-6, IL-1, PSP, and PCT were detected for each patient. Taste and Smell Questionnaire Section of the US NHANES 2011−2014 protocol (CDC 2013b) was used for gustatory function assessment. The study was approved by the Ethics committee of AOU Policlinico Consorziale di Bari (No. 6388 COVID19 DOM-protocol number 0034687/12-05-2020), and written informed consent was obtained. A total of 208 patients referred only to alteration to taste (208/821). 75/208 ageusia, 71/208 ipoageusia, 21/208 fantageusia, 19/208 dysgeusia, 22/208 parageusia. Significant correlations between CRP, IL-6, IL-1, PSP, PCT levels and type of dysfunctions about the perception of heat, cold and food consistency have not been found (P>0.05). Loss of taste can be due to the action of inflammatory mediators on gustatory buds, while alteration of cold, heat and food consistency perception may be due to direct damage of filiform papillae, allowing virus binding through the spike protein to ACE2 receptors of filiform papillae cells.
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause loss or alteration of taste and smell as early symptoms and sequelae, but the detailed mechanism remains unclear. This study investigated whether coronavirus disease 2019-induced taste disorders are caused by direct effects on taste bud cells. SARS-CoV-2 recombinant spike and nucleocapsid proteins were applied to circumvallate papillae of male Sprague-Dawley rats. Immunohistochemistry and image analysis were used to compare the number of taste buds, and taste bud cells and area, together with confirmation of angiotensin-converting enzyme 2 (ACE2) expression. Immunohistochemical analysis revealed ACE2 expression in the taste buds of rat circumvallate papillae. Decreases in the number of taste buds, taste bud cells, and their area were observed at 12 days after application of SARS-CoV-2 recombinant spike and nucleocapsid proteins. These data suggest that SARS-CoV-2 proteins induce degeneration of taste buds.