The inability to smell or taste became a distinctive and widely reported symptom of infection with SARS-CoV-2, the virus that causes COVID-19. Unlike the temporary congestion-related loss of smell experienced during a common cold, this symptom, medically termed anosmia (loss of smell) or ageusia (loss of taste), often occurred abruptly without any nasal blockage. This unique presentation quickly established itself as a common and sometimes the only early indicator of infection. The mechanism behind this sensory disruption is highly specific, targeting delicate structures within the nasal cavity rather than causing simple obstruction.
The Difference Between Taste and Smell
Most people who contract COVID-19 and lose their senses report that food has no “taste,” but the primary issue is actually a disruption of the sense of smell. True taste, or gustation, is limited to five basic sensations detected by taste buds on the tongue: sweet, sour, salty, bitter, and umami. These sensations remain largely intact for many patients with COVID-19.
Flavor perception is a much richer sensory experience that is dependent on the olfactory system. When eating, odor molecules travel up the back of the throat to the nose, a process known as retronasal olfaction. This combination of the five basic tastes from the tongue and the vast array of aromas from the nose is what the brain interprets as flavor. Without olfactory input, a person can distinguish between sweet and salty, but cannot identify the distinct flavor of chocolate or coffee.
How the Virus Disrupts Olfactory Supporting Cells
The scientific explanation for this sensory loss focuses on the cell types the virus targets within the nasal cavity. SARS-CoV-2 requires two tools to enter human cells: the Angiotensin-Converting Enzyme 2 (ACE2) receptor and the TMPRSS2 enzyme. These proteins allow the virus to breach the cell membrane.
Olfactory sensory neurons—the nerve cells responsible for detecting odors—do not express high concentrations of the ACE2 receptor. This means the virus generally cannot infect or directly destroy the nerve cells that sense smell. Instead, the virus targets the non-neuronal cells surrounding them, known as sustentacular cells, which are rich in ACE2 and TMPRSS2.
Sustentacular cells are the primary supporting cells of the olfactory system. They provide metabolic support, maintain tissue integrity, and regulate the chemical environment necessary for the neurons to fire correctly. When the virus infects and damages these supporting cells, the microenvironment surrounding the sensory neurons becomes compromised.
This damage leads to inflammation and dysfunction in the olfactory epithelium, preventing sensory neurons from sending accurate signals to the brain. The resulting anosmia is an indirect effect; the smell-detecting neurons are starved of the necessary support they need to function. Because the neurons themselves are spared direct infection, this mechanism explains why the loss of smell is often sudden and temporary for most patients.
Understanding Recovery and Distorted Senses
Since the core olfactory sensory neurons are not destroyed by the virus, the prognosis for recovering the sense of smell is favorable. Recovery occurs as sustentacular cells regenerate, restoring the healthy environment needed for sensory neurons to function. For most patients, recovery begins within a few weeks, though it can take several months to return to normal.
A significant number of people experience qualitative olfactory dysfunction during recovery. The two most common forms are parosmia and phantosmia. Parosmia is a distorted sense of smell where familiar odors are perceived as unpleasant, often described as smelling like sulfur or chemicals. Phantosmia is the experience of smelling something that is not actually there, known as a phantom odor.
These distorted perceptions are a sign of the olfactory nerves incorrectly reconnecting as the system repairs itself. Signals sent to the brain can be misinterpreted until the neural wiring is fully restored.