The loss of the sense of smell (anosmia) and taste (ageusia) became a distinctive symptom of infection with the SARS-CoV-2 virus, which causes COVID-19. This sensory disruption set the illness apart from many other respiratory viruses early in the pandemic. While the frequency of this symptom has changed significantly with new variants, it remains a recognized potential effect of a current COVID-19 infection.
Current Prevalence of Sensory Loss
The likelihood of experiencing a loss of smell or taste has dropped substantially since the beginning of the pandemic. Early in 2020, chemosensory loss was reported in a high percentage of COVID-19 cases, sometimes affecting up to 80% of infected individuals. This high prevalence made it a reliable indicator of infection during the initial waves.
The emergence of new variants has fundamentally shifted this pattern, making the symptom far less common. Comparative data shows a steep decline in the risk of losing smell or taste from Delta to Omicron variants. For instance, the risk of chemosensory loss with the Delta variant was approximately 44% lower than with the original strain.
The Omicron variant and its subsequent sub-lineages marked the most dramatic reduction in this particular symptom. The risk of experiencing smell or taste loss with Omicron infection was found to be as low as 6% to 7% of the risk observed during the initial waves. This decrease is attributed to changes in how the virus interacts with human cells, specifically a change in viral tropism.
The virus appears to have evolved to be less damaging to the olfactory epithelium, the tissue responsible for smell. Widespread immunity from vaccination and prior infections may also contribute to a milder immune response that lessens inflammation in the nasal passages. While not a universal symptom, a new loss of smell is still a possibility that should prompt testing for COVID-19.
The Biological Mechanism Behind Olfactory Disruption
The process through which the SARS-CoV-2 virus causes anosmia is specific and does not involve a direct attack on the olfactory neurons. The virus requires two elements to enter a cell: the Angiotensin-Converting Enzyme 2 (ACE2) receptor and the TMPRSS2 enzyme. These proteins are abundantly expressed on the supporting cells within the olfactory epithelium, known as sustentacular cells.
The virus primarily infects these sustentacular cells, which provide metabolic and structural support to the olfactory sensory neurons (OSNs). Infection of these supporting cells triggers a massive inflammatory response within the nasal cavity. This inflammation, characterized by the infiltration of immune cells, causes widespread damage to the surrounding tissue.
The damage and inflammation disrupt the structure and function of the OSNs, leading to a loss of the cilia on the neurons. Since these cilia bind odor molecules and initiate the signal to the brain, their damage effectively silences the sense of smell. This indirect mechanism explains why the loss can be sudden, profound, and often reversible as the supporting cells regenerate.
Clarifying the Difference Between Taste and Smell Loss
The common experience of “losing taste” during COVID-19 is usually a misinterpretation of a profound loss of flavor perception. True taste (ageusia) is the inability to detect the five basic qualities: sweet, sour, salty, bitter, and umami. These primary tastes are sensed by taste buds on the tongue and are less affected by the virus.
The richness of flavor, which allows a person to distinguish between foods, is driven by retronasal olfaction. This process involves odors from food in the mouth traveling up to the olfactory receptors in the nasal cavity. When anosmia occurs, this pathway is blocked, making food seem bland, flat, or tasteless.
While the vast majority of reported “taste loss” is a consequence of smell loss, some studies suggest the virus may cause a genuine, though less severe, reduction in true taste intensity. Even so, the sensory disruption from smell loss is significantly more pronounced than any potential direct effect on the taste receptors of the tongue. Therefore, the primary sensory issue in COVID-19 is anosmia.
Recovery Timelines and Management Techniques
For most individuals who experience anosmia due to COVID-19, the loss is temporary, with recovery beginning within a few weeks. A significant majority of patients (around 88%) report a return of their sense of smell within two months. However, a minority may face prolonged symptoms that persist for several months or, in rare cases, become chronic.
When the sense of smell returns, some people may experience a distorted sense of smell (parosmia) or phantom smells (phantosmia). Parosmia often causes formerly pleasant odors, like coffee, to smell foul, metallic, or repulsive. This is thought to be a sign of incorrectly reconnecting olfactory nerves. Phantosmia involves smelling odors that are not actually present.
The most effective, evidence-based management strategy for persistent smell loss is olfactory training. This technique involves smelling a set of four distinct, potent odors twice a day for several months. The goal is to stimulate the regenerating olfactory nerves and help retrain the brain to recognize the scents. The odors typically include:
- A flower (e.g., rose)
- A resin (e.g., eucalyptus)
- A fruit (e.g., lemon)
- A spice (e.g., clove)
An individual should seek medical evaluation from an ear, nose, and throat (ENT) specialist if the sense of smell has not returned or shown improvement after four weeks. While training can be done at home, a specialist can rule out other causes for the loss and may suggest treatments, such as nasal steroid sprays to reduce inflammation.