This hypothesis proposes that infection of olfactory sensory neurons (OSNs) is the basis of anosmia-related symptoms in COVID-19 patients.

1) SARS-CoV-2 binds to ACE2 in nasal and oral mucosa, inhibiting sensory receptor cells that mediate olfaction and gustation

2) SARS-CoV-2 crosses the cribriform plate and binds to neurons in the olfactory bulb, causing anosmia. The virus also moves from gustatory receptor cells in the tongue to damage neurons in the nucleus solitarius in medulla, leading to ageusia

Boston University

There has been speculation about the potential causes of anosmia and ageusia in COVID-19 patients. Two key MOAs have been proposed: a neuronal infection-based hypothesis and a non-neuronal infection-based hypothesis.

Potential Causes of Anosmia and Ageusia in COVID-19 Patients

Fotuhi, M., Mian, A., Meysami, S., & Raji, C. A. (2020). Neurobiology of COVID-19. Journal of Alzheimers Disease, 76(1), 3-19. doi:10.3233/jad-200581
https://content.iospress.com/articles/journal-of-alzheimers-disease/jad200581

Neurobiology of COVID-19

This hypothesis proposes that infection of olfactory epithelium (OE)-related cells, such as sustentacular and basal cells, is the basis of anosmia-related symptoms  in COVID-19 patients (Ref #1)

1) Gene expression profiles of human nasal biopsy samples revealed that neither ACE2 nor TMPRSS2 were detected in OSNs, which would be necessary for SARS-CoV-2 infection. This was confirmed by immunostaining of human biopsy tissue.

2) Immunostaining revealed, however, that OE cells such as sustentacular and basal cells express ACE2. This suggests that the MOA for COVID-19-mediated anosmia may be from damage of these OE cells.

3) These findings are confirmed by experiments performed in Syrian hamster models of SARS-CoV-2 infection (Ref #2)

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