Published version from the manuscript. Funding: This investigation was funded by grants in the National All-natural Science Foundation of China (81872228), the Guangdong Basic and Applied Standard Analysis Foundation (2020B1515020002). The funders had no part in the design and style with the study; within the collection, analyses, or interpretation of data; inside the writing from the manuscript, or within the selection to publish the results. Institutional Overview Board Statement: All of the animal experiments had been approved by the Institutional Animal Care and Use Committee of Sun Yat-sen University (reference no. L102042016110W), plus the animals have been handled in accordance with institutional suggestions. Informed Consent Statement: Not applicable. Data Availability Statement: The information presented in this study are readily available on request from the corresponding author.Viruses 2021, 13,12 ofAcknowledgments: We would like to thank the team at BEIJING IDMO Co., Ltd. for their technical assistance to create humanized mouse model. Conflicts of Interest: The authors declare no conflict of interest.
virusesReviewCOVID-19 Anosmia: Higher Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2Fengyi Liang 1, and De Yun WangHealthy Longevity Translational Study Plan, Division of Anatomy, Yong Loo Lin College of Medicine, National University of Singapore, Singapore 117594, Singapore Infectious Illnesses Translational Research Plan, Division of Otolaryngology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore; [email protected] Correspondence: [email protected]; Tel.: 65-6516-Citation: Liang, F.; Wang, D.Y. COVID-19 Anosmia: Higher Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of PHA-543613 Purity & Documentation SARS-CoV-2 Viruses 2021, 13, 2225. https://doi.org/ 10.3390/v13112225 Academic Editors: Kyung-Yil Lee and Seung-Beom Han Received: 30 September 2021 Accepted: 30 October 2021 Published: 4 NovemberAbstract: Extreme acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 2019 (COVID-19). It is generally known as a respiratory virus, but SARS-CoV-2 seems equally, and even a lot more, infectious for the olfactory epithelium (OE) than for the respiratory epithelium inside the nasal cavity. In light with the compact area of the OE relative for the respiratory epithelium, the high PK 11195 manufacturer Prevalence of olfactory dysfunctions (ODs) in COVID-19 has been bewildering and has attracted substantially focus. This evaluation aims to initially examine the cytological and molecular biological qualities in the OE, in particular the microvillous apical surfaces of sustentacular cells and the abundant SARS-CoV-2 receptor molecules thereof, that might underlie the high susceptibility of this neuroepithelium to SARS-CoV-2 infection and damages. The possibility of SARS-CoV-2 neurotropism, or the lack of it, is then analyzed with regard for the expression of the receptor (angiotensin-converting enzyme two) or priming protease (transmembrane serine protease two), and cellular targets of infection. Neuropathology of COVID-19 in the OE, olfactory bulb, along with other associated neural structures are also reviewed. Toward the end, we present our perspectives relating to possible mechanisms of SARS-CoV-2 neuropathogenesis and ODs, inside the absence of substantial viral infection of neurons. Plausible causes for persistent ODs in some COVID-19 convalescents are also examined. Keyword phrases: COVID-19; SARS-CoV-2; olfactory dysfunction; anosmia; pathogenesis1. Introduc.