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1.
Article in English | WPRIM (Western Pacific) | ID: wpr-999872

ABSTRACT

Olfaction is one of the five basic human senses, and it is known to be one of the most primitive senses. The sense of olfaction may have been critical for human survival in prehistoric society, and although many believe its importance has diminished over time, it continues to have an impact on human interaction, bonding, and propagation of the species. Even if we are unaware of it, the sense of smell greatly affects our lives and is closely related to overall quality of life and health. Nonetheless, olfaction has been neglected from a scientific perspective compared to other senses. However, olfaction has recently received substantial attention since the loss of smell and taste has been noted as a key symptom of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Studies investigating olfaction loss in association with coronavirus disease 2019 (COVID-19) have revealed that olfactory dysfunction can be both conductive and sensorineural, possibly causing structural changes in the brain. Olfactory training is an effective treatment for olfactory dysfunction, suggesting the reorganization of neural associations. A reduced ability to smell may also alert suspicion for neurodegenerative or psychiatric disorders. Here, we summarize the basic knowledge that we, as otorhinolaryngologists, should have about the sense of smell and the peripheral and central olfactory pathways for managing and helping patients with olfactory dysfunction.

2.
Preprint in English | medRxiv | ID: ppmedrxiv-20092866

ABSTRACT

We investigated the expression and subcellular localization of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper (nasal) and lower (pulmonary) respiratory tracts of healthy human donors. We detected ACE2 protein expression within the cilia organelle of ciliated airway epithelial cells, which likely represents the initial or early subcellular site of SARS-CoV-2 viral entry during respiratory transmission. We further determined whether ACE2 expression in the cilia of upper respiratory cells was influenced by patient demographics, clinical characteristics, co-morbidities, or medication use, and found no evidence that the use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) increases ACE2 protein expression.

3.
Valentina Parma; Kathrin Ohla; Maria G. Veldhuizen; Masha Y. Niv; Christine E. Kelly; Alyssa J. Bakke; Keiland W. Cooper; Cédric Bouysset; Nicola Pirastu; Michele Dibattista; Rishemjit Kaur; Marco Tullio Liuzza; Marta Y. Pepino; Veronika Schöpf; Veronica Pereda-Loth; Shannon B Olsson; Richard C Gerkin; Paloma Rohlfs Domínguez; Javier Albayay; Michael C. Farruggia; Surabhi Bhutani; Alexander W Fjaeldstad; Ritesh Kumar; Anna Menini; Moustafa Bensafi; Mari Sandell; Iordanis Konstantinidis; Antonella Di Pizio; Federica Genovese; Lina Öztürk; Thierry Thomas-Danguin; Johannes Frasnelli; Sanne Boesveldt; Özlem Saatci; Luis R. Saraiva; Cailu Lin; Jérôme Golebiowski; Liang-Dar Hwang; Mehmet Hakan Ozdener; Maria Dolors Guàrdia; Christophe Laudamiel; Marina Ritchie; Jan Havlícek; Denis Pierron; Eugeni Roura; Marta Navarro; Alissa A. Nolden; Juyun Lim; KL Whitcroft; Lauren R. Colquitt; Camille Ferdenzi; Evelyn V. Brindha; Aytug Altundag; Alberto Macchi; Alexia Nunez-Parra; Zara M. Patel; Sébastien Fiorucci; Carl M. Philpott; Barry C. Smith; Johan N Lundström; Carla Mucignat; Jane K. Parker; Mirjam van den Brink; Michael Schmuker; Florian Ph.S Fischmeister; Thomas Heinbockel; Vonnie D.C. Shields; Farhoud Faraji; Enrique Enrique Santamaría; William E.A. Fredborg; Gabriella Morini; Jonas K. Olofsson; Maryam Jalessi; Noam Karni; Anna D'Errico; Rafieh Alizadeh; Robert Pellegrino; Pablo Meyer; Caroline Huart; Ben Chen; Graciela M. Soler; Mohammed K. Alwashahi; Olagunju Abdulrahman; Antje Welge-Lüssen; Pamela Dalton; Jessica Freiherr; Carol H. Yan; Jasper H. B. de Groot; Vera V. Voznessenskaya; Hadar Klein; Jingguo Chen; Masako Okamoto; Elizabeth A. Sell; Preet Bano Singh; Julie Walsh-Messinger; Nicholas S. Archer; Sachiko Koyama; Vincent Deary; S. Craig Roberts; Hüseyin Yanik; Samet Albayrak; Lenka Martinec Novákov; Ilja Croijmans; Patricia Portillo Mazal; Shima T. Moein; Eitan Margulis; Coralie Mignot; Sajidxa Mariño; Dejan Georgiev; Pavan K. Kaushik; Bettina Malnic; Hong Wang; Shima Seyed-Allaei; Nur Yoluk; Sara Razzaghi; Jeb M. Justice; Diego Restrepo; Julien W Hsieh; Danielle R. Reed; Thomas Hummel; Steven D Munger; John E Hayes.
Preprint in English | medRxiv | ID: ppmedrxiv-20090902

ABSTRACT

Recent anecdotal and scientific reports have provided evidence of a link between COVID-19 and chemosensory impairments such as anosmia. However, these reports have downplayed or failed to distinguish potential effects on taste, ignored chemesthesis, generally lacked quantitative measurements, were mostly restricted to data from single countries. Here, we report the development, implementation and initial results of a multi-lingual, international questionnaire to assess self-reported quantity and quality of perception in three distinct chemosensory modalities (smell, taste, and chemesthesis) before and during COVID-19. In the first 11 days after questionnaire launch, 4039 participants (2913 women, 1118 men, 8 other, ages 19-79) reported a COVID-19 diagnosis either via laboratory tests or clinical assessment. Importantly, smell, taste and chemesthetic function were each significantly reduced compared to their status before the disease. Difference scores (maximum possible change {+/-}100) revealed a mean reduction of smell (-79.7 {+/-} 28.7, mean {+/-} SD), taste (-69.0 {+/-} 32.6), and chemesthetic (-37.3 {+/-} 36.2) function during COVID-19. Qualitative changes in olfactory ability (parosmia and phantosmia) were relatively rare and correlated with smell loss. Importantly, perceived nasal obstruction did not account for smell loss. Furthermore, chemosensory impairments were similar between participants in the laboratory test and clinical assessment groups. These results show that COVID-19-associated chemosensory impairment is not limited to smell, but also affects taste and chemesthesis. The multimodal impact of COVID-19 and lack of perceived nasal obstruction suggest that SARS-CoV-2 infection may disrupt sensory-neural mechanisms.

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