The COVID-19 pandemic introduced a wide range of symptoms, with one of the most distinctive being the sudden loss of the chemical senses, taste and smell. This phenomenon, known as chemosensory loss, was reported by a majority of individuals diagnosed with the virus, often serving as one of the earliest indicators of infection. While the inability to perceive the complex flavor of food caused significant distress, the effect on the basic sense of taste, including the perception of salt, presented a nuanced question for researchers. This sensory disruption highlighted the complex biological interplay between our senses of smell and taste.
Salt Taste Perception During Infection
The ability to detect the basic taste of salt often remains partially functional, even when the overall flavor of salty foods is severely diminished. True taste, known as gustation, involves five primary sensations: sweet, sour, bitter, umami, and salty. Studies have shown that while the perception of other basic tastes like sweet, sour, and bitter can be impaired, the detection threshold for salt may be less affected. In some cases, patients even report a hypersensitivity to salt.
This apparent preservation of the salt sensation is misleading, as the flavor experience of a salty dish relies heavily on smell. A person can still register the chemical sensation of sodium chloride on the tongue, but without the accompanying aroma, the food tastes flat and unrecognizable. For instance, someone might recognize the saltiness of a pretzel but completely miss the flavor notes of the butter, yeast, or baking process. This distinction explains why patients often report a near-total loss of “taste,” when they are primarily experiencing a loss of smell-driven flavor.
The Difference Between True Taste Loss and Smell-Related Loss
Chemosensory perception is divided into two distinct biological systems: olfaction and gustation. Olfaction, or the sense of smell, is responsible for detecting volatile chemical compounds in the air, which we experience as aroma. When we chew food, these aromatic molecules travel up the back of the throat to the olfactory epithelium in a process called retronasal smell, which is the source of complex flavor perception.
Gustation, or true taste, is mediated by specialized cells on the tongue that are organized into taste buds. These cells detect non-volatile chemicals that dissolve in saliva, allowing for the perception of the basic tastes. The virus appears to affect the sense of smell far more frequently and profoundly than the sense of taste. Some studies show that while nearly all patients experience some degree of olfactory loss, gustatory deficits are reported less often.
When taste loss, or hypogeusia, does occur, it is often a reduction in sensitivity across several of the basic tastes, rather than a total inability to taste. The basic salty taste is detected by epithelial sodium channels (ENaC) on the taste cells, which facilitate the movement of sodium ions. Research suggests that components of the virus may interact with proteins in taste cells, such as ACE2, which is part of a system that regulates salt balance and blood pressure. This interaction could potentially disrupt the sensitivity of the salt-sensing channels, leading to either a diminished or, paradoxically, a heightened perception of saltiness.
Biological Mechanisms Behind Chemosensory Dysfunction
The primary cause of the sensory loss is the virus’s interaction with specific cells in the olfactory epithelium, the tissue lining the roof of the nasal cavity. The SARS-CoV-2 virus uses the Angiotensin-Converting Enzyme 2 (ACE2) receptor and the TMPRSS2 enzyme to enter human cells. These entry points are highly expressed in the sustentacular cells, which are non-neuronal supporting cells in the olfactory tissue.
The olfactory sensory neurons themselves, which transmit smell signals to the brain, do not express high levels of the ACE2 receptor. Therefore, the virus does not typically destroy the sensory neurons directly. Instead, damage to the surrounding sustentacular cells causes structural and metabolic support disruption, leading to temporary dysfunction or death of the sensory neurons.
This indirect damage mechanism explains why the loss of smell is often sudden, profound, and typically reversible. For gustation, the mechanism is less clear, but the presence of ACE2 in taste cells suggests a potential direct viral effect on the tongue. The inflammatory response triggered by the infection, including elevated levels of immune signaling molecules, may also contribute to the temporary impairment of taste perception. The resulting chemosensory dysfunction is a combination of direct viral interaction and secondary inflammatory effects.
Recovery Timelines and Management
For most individuals, chemosensory function returns relatively quickly, with a majority of patients reporting recovery of smell and taste within a few weeks to two months. The median recovery time for taste is often reported to be around ten to twelve days, which is slightly faster than the recovery for smell. However, a substantial number of people experience prolonged symptoms, with some degree of olfactory dysfunction persisting for several months or longer.
During the recovery phase, some patients may develop parosmia, a condition where odors are perceived as distorted and often unpleasant, such as smelling foul or burnt chemicals instead of normal scents. Less commonly, phantosmia, or the perception of phantom smells that are not actually present, can also occur. The most established management technique for persistent smell loss is olfactory training, which involves the repetitive, conscious sniffing of a set of four distinct odors. This training aims to encourage the regeneration and reorganization of the olfactory system, offering a non-pharmacological path toward functional recovery.