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More that ACE2? NRP1 may play a central role in the underlying pathophysiological mechanism of olfactory dysfunction in COVID-19 and its association with enhanced survival.
Hopkins, Claire; Lechien, Jerome R; Saussez, Sven.
  • Hopkins C; Guy's and St Thomas NHS Foundation Trust, London, UK; King's College, London, UK. Electronic address: claire.hopkins@gstt.nhs.uk.
  • Lechien JR; COVID-19 Task Force of the Young-Otolaryngologists of the International Federations of Oto-rhino-laryngological Societies (YO-IFOS), Paris, France; Department of Human Anatomy and Experimental Oncology, Faculty of Medicine, UMONS Research Institute for Health Sciences and Technology, University of Mons (UMons), Mons, Belgium; Department of Otorhinolaryngology and Head and Neck Surgery, CHU Saint-Pierre, School of Medicine, CHU de Bruxelles, Université Libre de Bruxelles, Brussels, Belgium; Depar
  • Saussez S; COVID-19 Task Force of the Young-Otolaryngologists of the International Federations of Oto-rhino-laryngological Societies (YO-IFOS), Paris, France; Department of Human Anatomy and Experimental Oncology, Faculty of Medicine, UMONS Research Institute for Health Sciences and Technology, University of Mons (UMons), Mons, Belgium; Department of Otorhinolaryngology and Head and Neck Surgery, CHU Saint-Pierre, School of Medicine, CHU de Bruxelles, Université Libre de Bruxelles, Brussels, Belgium.
Med Hypotheses ; 146: 110406, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-939150
ABSTRACT
Three mechanisms have been proposed to account for COVID-19 associated olfactory dysfunction; obstruction of the olfactory cleft; epithelial injury and infection of the sustentacular supporting cells, which are known to express ACE2, or injury to the olfactory bulb due to axonal transport through olfactory sensory neurones. The absence of ACE2 expression by olfactory sensory neurones has led to the neurotropic potential of COVID-19 to be discounted. While an accumulating body of evidence supports olfactory epithelial injury as an important mechanism, this does not account for all the features of olfactory dysfunction seen in COVID-19; for example the duration of loss in some patients, evidence of changes within the olfactory bulb on MRI imaging, identification of viral particles within the olfactory bulb in post-mortem specimens and the inverse association between severity of COVID-19 and the prevalence of olfactory loss. The recent identification of a second route of viral entry mediated by NRP1 addresses many of these inconsistencies. Expression by the olfactory sensory neurones and their progenitor cells may facilitate direct injury and axonal transport to the olfactory bulb as well as a mechanism for delayed or absent recovery. Expression by regulatory T cells may play a central role in the cytokine storm. Variability in expression by age, race or gender may explain differing morbidity of infection and inverse association between anosmia and severity; in the case of higher expression there may be a higher risk of olfactory function but greater activation of regulatory T cells that may suppress the cytokine storm.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Neuropilin-1 / Angiotensin-Converting Enzyme 2 / SARS-CoV-2 / COVID-19 / Olfaction Disorders / Models, Biological Type of study: Observational study / Prognostic study Topics: Long Covid Limits: Humans Language: English Journal: Med Hypotheses Year: 2021 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Neuropilin-1 / Angiotensin-Converting Enzyme 2 / SARS-CoV-2 / COVID-19 / Olfaction Disorders / Models, Biological Type of study: Observational study / Prognostic study Topics: Long Covid Limits: Humans Language: English Journal: Med Hypotheses Year: 2021 Document Type: Article