COVID 19-Induced Smell and Taste Impairments: Putative Impact on Physiology

Abstract

Smell and taste impairments are recognized as common symptoms in COVID 19 patients even in an asymptomatic phase. Indeed, depending on the country, in up to 85-90% of cases anosmia and dysgeusia are reported. We will review briefly the main mechanisms involved in the physiology of olfaction and taste focusing on receptors and transduction as well as the main neuroanatomical pathways. Then we will examine the current evidences, even if still fragmented and unsystematic, explaining the disturbances and mode of action of the virus at the level of the nasal and oral cavities. We will focus on its impact on the peripheral and central nervous system. Finally, considering the role of smell and taste in numerous physiological functions, especially in ingestive behavior, we will discuss the consequences on the physiology of the patients as well as management regarding food intake.

Keywords: COVID 19; feeding behavior; physiopathology; smell; taste.

FIGURE 1

Anatomy of taste and olfaction. Volatile odorant molecules are detected by olfactory sensory neurons (OSNs) located in the olfactory epithelium. OSNs are neurons extending ciliated dendrites in the periphery and with axons forming synapses with glomeruli in the olfactory bulbs situated in the brain. Taste buds located on the tongue are involved in the detection of soluble tasting compounds. The detection is achieved by taste receptor cells located in taste buds. Taste information is transmitted to the brain by three nerves, including chorda tympani, the glossopharyngeal, and the vagus nerves.

FIGURE 2

A model for anosmia based on hamsters studies. Sustentacular cells are the main target of SARS-CoV-2 infection. Two to four days post-infection (dpi), the virus is present mainly in these cells. The massive infection of sustentacular cells is followed by a desquamation of the olfactory epithelium which is simultaneously invaded by activated immunity cells. The desquamation is visible through a reduced thickness of the olfactory epithelium and presence of cellular debris in the lumen of the nasal cavity. The cellular aggregates contain sustentacular cells, activated immune cells as well as olfactory neurons. In the non-desquamated zone, the olfactory neurons are losing their dendrite. Seven days post-infection, the olfactory epithelium is already regenerating due to basal cells in healthy individuals and injured olfactory sensory neurons could recover their dendrite layer. If initial virus load is high or in overweight/aged individuals whose initial integrity of the olfactory epithelium may already be impaired, the regeneration of the olfactory epithelium may be less efficient. This could lead to secondary infection of olfactory neurons as well as a slower recovery of the olfactory epithelium function. Part of the olfactory epithelium could also be replaced by respiratory epithelium following the massive inflammation.

FIGURE 3

Hedonic sensory signal and food intake. Signals coming from the chemosensory systems (olfaction, taste, and chemesthesis) directly inform the brain of the sensory quality of food. The main brain areas involved are those of the reward system as well as hypothalamic nuclei. These will be involved in different components of feeding behavior such as motivation and pleasure to eat but also sensory specific appetite and satiation.