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Innate immune signaling in the olfactory epithelium reduces odorant receptor levels: modeling transient smell loss in COVID-19 patients

Rodriguez, S.; Cao, L.; Rickenbacher, G. T.; Benz, E. G.; Magdamo, C.; Ramirez Gomez, L. A.; Holbrook, E.; Dhilla Albers, A.; Gallagher, R.; Westover, M. B.; Evans, K. E.; Tatar, D.; Mukerji, S.; Zafonte, R.; Boyer, E. W.; Yu, C. R.; Albers, M. W.

2020-06-16 neurology
10.1101/2020.06.14.20131128 medRxiv
Show abstract

Post-infectious anosmias typically follow death of olfactory sensory neurons (OSNs) with a months-long recovery phase associated with parosmias. While profound anosmia is the leading symptom associated with COVID-19 infection, many patients regain olfactory function within days to weeks without distortions. Here, we demonstrate that sterile induction of anti-viral type I interferon signaling in the mouse olfactory epithelium is associated with diminished odor discrimination and reduced odor-evoked local field potentials. RNA levels of all class I, class II, and TAAR odorant receptors are markedly reduced in OSNs in a non-cell autonomous manner. We find that people infected with COVID-19 rate odors with lower intensities and have odor discrimination deficits relative to people that tested negative for COVID-19. Taken together, we propose that inflammatory-mediated loss of odorant receptor expression with preserved circuit integrity accounts for the profound anosmia and rapid recovery of olfactory function without parosmias caused by COVID-19.

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