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1.
Preprint in English | bioRxiv | ID: ppbiorxiv-164335

ABSTRACT

ObjectivesIntracellular entry of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) depends on the interaction between its spike protein to a cellular receptor named angiotensin-converting enzyme 2 (ACE2) and depends on Furin-mediated spike 23 protein cleavage and spike protein priming by host cell proteases including 24 transmembrane protease serine 2 (TMPRSS2). Tmprss1, Tmprss3, and Tmprss5 are expressed in the spiral ganglion neurons and the organ of Corti in the inner ear; however, Ace2, Tmprss2, and Furin expression profiles in the middle ear remain unclear. Therefore, this study aimed to analyze Ace2, Tmprss2, and Furin expression in the middle and inner ear of mice. Study DesignAnimal research. SettingDepartment of Otolaryngology and Head and Neck Surgery, University of Tokyo. MethodsWe performed immunohistochemical analysis to examine the distribution of Ace2, Tmprss2, and Furin in the eustachian tube, middle ear space, and cochlea of mice. ResultsAce2 was expressed in the cytoplasm in the middle ear epithelium, eustachian tube epithelium, stria vascularis, and spiral ganglion. Tmprss2 and Furin were widely expressed in the middle ear spaces and the cochlea. ConclusionCo-expression of Ace2, Tmprss2, and Furin in the middle ear indicates that the middle ear is susceptible to SARS-CoV-2 infections, thus warranting the use of personal protective equipment during mastoidectomy for coronavirus disease (COVID-19) patients.

2.
Preprint in English | bioRxiv | ID: ppbiorxiv-097352

ABSTRACT

Background Anosmia is a frequent symptom in patients with the coronavirus disease 2019 (COVID-19) driven by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and mostly recovers within weeks. This clinical figure is significantly different from that of anosmia after upper respiratory infection, which occurs in only a small proportion of patients and does not recover or requires months to recover. The background mechanisms of COVID-19 induced olfactory dysfunction have not been elucidated.Methods To address the unique pathophysiology of olfactory dysfunction associated with COVID-19, we examined the existence and distribution of ACE2 (virus binding receptor), TMPRSS2 and Furin (proteases to facilitate virus entry) in the nasal mucosa, composed of the respiratory mucosa (RM) and olfactory mucosa (OM), and the olfactory bulb (OB) in mouse and human tissues by immunohistochemistry and gene analyses.Results Ace2, Tmprss2, and Furin gene expressions were confirmed in the nasal mucosa and OB. ACE2 was widely expressed all in the RM, OM and OB. Co-expression of ACE2, TMPRSS2, and Furin was observed in the RM including the RE and subepithelial glands and in the OM, especially in the supporting cells on the olfactory epithelium and the Bowman’s glands. Notably, the olfactory receptor neurons (ORNs) in the OM were positive for ACE2 but almost negative for TMPRSS2 and Furin. The cells in the OB expressed ACE2 strongly and Furin weakly and did not express TMPRSS2.Conclusions ACE2 was widely expressed in the RM, OM and OB, but TMPRSS2 and Furin were expressed in certain types of cells and were absent in the ORNs. These findings, together with clinically reported ones, suggest that COVID-19 related anosmia can occur due to mainly sensorineural and central dysfunction and, to some extent, conductive olfactory dysfunction. That the ORNs express ACE2 but not TMPRSS2 or Furin may explain the early recovery of anosmia.Short Summary Protein expression patterns of ACE2, TMPRSS, and Furin suggest that COVID-19 related anosmia can occur due to mainly sensorineural dysfunction without olfactory neuronal damage.Competing Interest StatementThe authors have declared no competing interest.View Full Text

3.
Preprint in English | bioRxiv | ID: ppbiorxiv-097204

ABSTRACT

Objective Patients with coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibit not only respiratory symptoms but also symptoms of chemo-sensitive disorders and kidney failure. Cellular entry of SARS-CoV-2 depends on the binding of its spike protein to a cellular receptor named angiotensin-converting enzyme 2 (ACE2), and the subsequent spike protein-priming by host cell proteases, including transmembrane protease serine 2 (TMPRSS2). Thus, high expression of ACE2 and TMPRSS2 are considered to enhance the invading capacity of SARS-CoV-2.Methods To elucidate the underlying histological mechanisms of the aerodigestive disorders caused by SARS-CoV-2, we investigated the expression of ACE2 and TMPRSS2 proteins in the aerodigestive tracts of the tongue, hard palate with partial nasal tissue, larynx with hypopharynx, trachea, esophagus, lung, and kidney of rats through immunohistochemistry.Results Strong co-expression of ACE2 and TMPRSS2 proteins was observed in the nasal respiratory epithelium, trachea, bronchioles, alveoli, kidney, and taste buds of the tongue. Remarkably, TMPRSS2 expression was much stronger in the peripheral alveoli than in the central alveoli. These results coincide with the reported clinical symptoms of COVID-19, such as the loss of taste, loss of olfaction, respiratory dysfunction, and acute nephropathy.Conclusions A wide range of organs have been speculated to be affected by SARS-CoV-2 depending on the expression levels of ACE2 and TMPRSS2. Differential distribution of TMPRSS2 in the lung indicated the COVID-19 symptoms to possibly be exacerbated by TMPRSS2 expression. This study might provide potential clues for further investigation of the pathogenesis of COVID-19.Level of Evidence NACompeting Interest StatementThe authors have declared no competing interest.View Full Text

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