COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 2019 (COVID-19). It is known as a respiratory virus, but SARS-CoV-2 appears equally, or even more, infectious for the olfactory epithelium (OE) than for the respiratory epithelium in the nas...

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Autores principales: Fengyi Liang, De Yun Wang
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/b8222442ca7041e5a1ff7696e63f9dca
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spelling oai:doaj.org-article:b8222442ca7041e5a1ff7696e63f9dca2021-11-25T19:13:29ZCOVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?10.3390/v131122251999-4915https://doaj.org/article/b8222442ca7041e5a1ff7696e63f9dca2021-11-01T00:00:00Zhttps://www.mdpi.com/1999-4915/13/11/2225https://doaj.org/toc/1999-4915Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 2019 (COVID-19). It is known as a respiratory virus, but SARS-CoV-2 appears equally, or even more, infectious for the olfactory epithelium (OE) than for the respiratory epithelium in the nasal cavity. In light of the small area of the OE relative to the respiratory epithelium, the high prevalence of olfactory dysfunctions (ODs) in COVID-19 has been bewildering and has attracted much attention. This review aims to first examine the cytological and molecular biological characteristics of the OE, especially the microvillous apical surfaces of sustentacular cells and the abundant SARS-CoV-2 receptor molecules thereof, that may 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 to the expression of the receptor (angiotensin-converting enzyme 2) or priming protease (transmembrane serine protease 2), and cellular targets of infection. Neuropathology of COVID-19 in the OE, olfactory bulb, and other related neural structures are also reviewed. Toward the end, we present our perspectives regarding possible mechanisms of SARS-CoV-2 neuropathogenesis and ODs, in the absence of substantial viral infection of neurons. Plausible causes for persistent ODs in some COVID-19 convalescents are also examined.Fengyi LiangDe Yun WangMDPI AGarticleCOVID-19SARS-CoV-2olfactory dysfunctionanosmiapathogenesisMicrobiologyQR1-502ENViruses, Vol 13, Iss 2225, p 2225 (2021)
institution DOAJ
collection DOAJ
language EN
topic COVID-19
SARS-CoV-2
olfactory dysfunction
anosmia
pathogenesis
Microbiology
QR1-502
spellingShingle COVID-19
SARS-CoV-2
olfactory dysfunction
anosmia
pathogenesis
Microbiology
QR1-502
Fengyi Liang
De Yun Wang
COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
description Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 2019 (COVID-19). It is known as a respiratory virus, but SARS-CoV-2 appears equally, or even more, infectious for the olfactory epithelium (OE) than for the respiratory epithelium in the nasal cavity. In light of the small area of the OE relative to the respiratory epithelium, the high prevalence of olfactory dysfunctions (ODs) in COVID-19 has been bewildering and has attracted much attention. This review aims to first examine the cytological and molecular biological characteristics of the OE, especially the microvillous apical surfaces of sustentacular cells and the abundant SARS-CoV-2 receptor molecules thereof, that may 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 to the expression of the receptor (angiotensin-converting enzyme 2) or priming protease (transmembrane serine protease 2), and cellular targets of infection. Neuropathology of COVID-19 in the OE, olfactory bulb, and other related neural structures are also reviewed. Toward the end, we present our perspectives regarding possible mechanisms of SARS-CoV-2 neuropathogenesis and ODs, in the absence of substantial viral infection of neurons. Plausible causes for persistent ODs in some COVID-19 convalescents are also examined.
format article
author Fengyi Liang
De Yun Wang
author_facet Fengyi Liang
De Yun Wang
author_sort Fengyi Liang
title COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
title_short COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
title_full COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
title_fullStr COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
title_full_unstemmed COVID-19 Anosmia: High Prevalence, Plural Neuropathogenic Mechanisms, and Scarce Neurotropism of SARS-CoV-2?
title_sort covid-19 anosmia: high prevalence, plural neuropathogenic mechanisms, and scarce neurotropism of sars-cov-2?
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/b8222442ca7041e5a1ff7696e63f9dca
work_keys_str_mv AT fengyiliang covid19anosmiahighprevalencepluralneuropathogenicmechanismsandscarceneurotropismofsarscov2
AT deyunwang covid19anosmiahighprevalencepluralneuropathogenicmechanismsandscarceneurotropismofsarscov2
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