Chemosensory loss in COVID-19

Abstract

The COVID-19 pandemic caused by SARS-CoV-2 virus quickly spread globally, infecting over half a billion individuals, and killing over 6 million*. One of the more unusual symptoms was patients' complaints of sudden loss of smell and/or taste, a symptom that has become more apparent as the virus mutated into different variants. Anosmia and ageusia, the loss of smell and taste, respectively, seem to be transient for some individuals, but for others persists even after recovery from the infection. Causes for COVID-19-associated chemosensory loss have undergone several hypotheses. These include non-functional or destroyed olfactory neurons and gustatory receptors or of their supporting cells, disruption of the signaling protein Neuropilin-1, and disruption in the interaction with semaphorins, key molecules in the gustatory and olfactory axon guidance. The current paper will review these hypotheses and chart out potential therapeutic avenues.

Keywords: COVID-19; SARS CoV-2; chemosensory disorders; olfaction; smell loss; taste; taste loss.

FIGURE 1

Structure of a taste bud (Spielman et al., , reproduced with permission of John Wiley & Sons)

FIGURE 2

Olfactory neuroepithelium in health and in COVID‐19‐induced anosmia

FIGURE 3

Thin sections from taste papillae and intestine of healthy (control) (a–d) and COVID+ (e, f) individuals were stained either with hematoxylin and eosin (a, b), or anti‐SARS‐CoV‐2 nucleocapsid antibodies (e, f; Invitrogen cat # PA5‐114532, 0.2 μg/ml, 4°C overnight). Image magnified at 40× obj. (Sunavala‐Dossabhoy and Spielman, unpublished)

FIGURE 4

Inflammatory cytokine theory of ageusia