The experience of losing the ability to smell and taste is a distinguishing characteristic of infection with the SARS-CoV-2 virus, which causes COVID-19. This sudden disappearance of the senses is clinically termed anosmia for the loss of smell and ageusia for the loss of taste. Unlike the temporary loss of smell that accompanies a common cold and congestion, this symptom often appears abruptly and can be an early indicator of infection, even in the absence of other respiratory issues. Understanding this unique symptom requires looking at the precise biological mechanisms being targeted by the virus. This involves a highly specific cellular attack within the nasal cavity, which explains why the sense of smell is affected so profoundly.
The Difference Between Taste and Smell
While patients often report losing both their sense of taste and smell, the primary issue is almost always a dysfunction of the olfactory system. True taste, or gustation, is limited to the perception of five basic qualities: sweet, sour, salty, bitter, and umami. The receptor cells for these tastes are located on the tongue and are not the main target of the virus.
The complex perception of “flavor” is an intricate combination of taste, texture, temperature, and, most importantly, smell. When you chew and swallow food, volatile odor molecules travel from the mouth up the throat and into the nasal cavity, a process known as retronasal olfaction. This pathway allows the brain to combine the basic taste signals from the tongue with the detailed olfactory information, creating the rich experience of flavor.
Because the olfactory system is responsible for detecting the thousands of complex odor profiles, the loss of smell effectively wipes out the perception of flavor. The tongue may still register saltiness or sweetness, but the nuanced difference between a lemon and a lime, or coffee and chocolate, is gone. Therefore, the reported loss of taste is largely a consequence of the severe disruption to the sense of smell.
The Cellular Mechanism of Smell Loss
The cause of this olfactory failure is a highly specific interaction between the SARS-CoV-2 virus and certain cells within the nasal epithelium. For the virus to gain entry into a human cell, it must first bind to a receptor protein called Angiotensin-Converting Enzyme 2 (ACE2), which acts like a cellular docking station. Viral entry is then facilitated by a second protein, the enzyme TMPRSS2, which helps cleave the viral spike protein.
Crucially, studies have shown that the olfactory sensory neurons themselves—the actual nerve cells that detect odors—do not express the ACE2 receptor. Instead, the virus targets the adjacent sustentacular cells, which are a type of supporting cell in the olfactory epithelium. These non-neuronal cells are rich in the necessary ACE2 and TMPRSS2 proteins, making them the primary site of infection.
Infection of the sustentacular cells causes inflammation and damage to these vital supporting structures. These cells are necessary for the function and metabolic support of the neighboring olfactory sensory neurons, which send smell signals to the brain. When the supporting cells are damaged, the nearby neurons become severely impaired or lose function, leading to the rapid onset of anosmia.
This mechanism differs significantly from the smell loss that happens during a typical cold or flu. In those cases, the loss of smell is generally due to physical congestion that blocks odor molecules from reaching the nerve cells. With COVID-19, the inflammation directly attacks the fundamental supporting infrastructure of the olfactory system, causing a more profound and distinct type of sensory loss.
The Recovery Process and Timeline
For many individuals, the loss of smell and flavor is temporary, with most people regaining their full sense within a few weeks to months. Recovery is possible because the olfactory sensory neurons, which were functionally impaired rather than directly destroyed by the virus, have a natural capacity for regeneration. The damage to the supporting sustentacular cells triggers a repair process where new supporting cells and neurons can be generated.
However, this regeneration process does not always occur smoothly, which can lead to lingering sensory distortions. One common distortion is parosmia, where previously normal odors are perceived as unpleasant, often smelling rotten, metallic, or burnt. This distortion is believed to happen because the regenerating olfactory neurons are making new, but incorrect, connections to the brain’s olfactory bulb.
A less common distortion, phantosmia, involves smelling things that are not actually present in the environment. Both parosmia and phantosmia are indicators that the olfactory system is actively misfiring as it attempts to reconnect and reorganize itself. While frustrating, these symptoms are often considered a positive sign of a system trying to heal.
To stimulate and guide this recovery, many specialists recommend olfactory training, also known as smell therapy. This involves intentionally sniffing a series of four distinct scents—typically including a fruity, floral, spicy, and resinous odor—twice a day for an extended period. This consistent, deliberate exposure helps the regenerating neurons relearn and correctly map the different odor profiles, aiding the system in restoring accurate function.