Anosmia, the complete or partial loss of smell, was one of the most distinctive symptoms of early COVID-19 infection. During the initial waves of the pandemic, this sudden sensory change frequently served as a strong indicator of infection. The nature of the virus has changed significantly over time, prompting questions about whether this symptom remains common. The evolution of SARS-CoV-2 variants has altered the typical presentation of the illness, shifting its pathology in the respiratory system.
Current Prevalence of Smell Loss
While the loss of smell is still possible with SARS-CoV-2 infection, its frequency has dramatically decreased compared to the virus’s ancestral strains. Early in the pandemic, up to 80% of infected individuals experienced some form of olfactory dysfunction. This symptom is now far less common with the currently circulating Omicron-derived variants. Modern data suggests the global prevalence of anosmia with the Omicron lineage is estimated to be around 3.7% in adults, representing a significant reduction from earlier variants like Alpha and Delta. This sharp decline means that while anosmia can still be a symptom, it is no longer the widespread feature it once was.
Why Newer Variants Cause Less Anosmia
The decreased incidence of smell loss is due to changes in the virus’s preferred site of infection, known as viral tropism. Earlier SARS-CoV-2 variants, such as the ancestral strain and Delta, showed a high affinity for cells in the olfactory epithelium located high up in the nasal cavity. This preference led to direct damage and inflammation in the region responsible for scent perception. Newer variants, including the Omicron sublineages, contain spike protein mutations that favor replication lower down in the respiratory tract, specifically in the cells of the bronchi and trachea. By shifting the primary site of replication away from the olfactory epithelium, the newer strains are less likely to trigger the local inflammation that causes anosmia.
The Biology of COVID-19 Smell Disruption
When anosmia occurs, the underlying mechanism is not due to the virus directly killing the olfactory sensory neurons. Instead, the virus targets non-neuronal supporting cells within the olfactory epithelium called sustentacular cells. These cells express high levels of the ACE2 receptor, which the virus uses as an entry point. Once infected, these supporting cells become damaged and release pro-inflammatory signaling molecules called cytokines. This intense local inflammation disrupts the function of the adjacent olfactory sensory neurons, which detect odors, causing the cilia on the neurons to retract or be damaged and temporarily eliminating the ability to smell.
Duration and Recovery of Smell Loss
For the majority of individuals who experience COVID-19-related smell loss, the symptom is temporary and resolves within a few weeks to a few months. A small percentage of patients, however, experience persistent olfactory dysfunction that can last six months or longer.
Individuals in recovery may also experience qualitative distortions of smell, such as parosmia or phantosmia. Parosmia involves perceiving familiar odors as unpleasant or distorted, while phantosmia is the perception of a smell when none is actually present.
The most common method to encourage recovery for persistent smell loss is olfactory training. This involves the regular, mindful sniffing of a set of four distinct odors to stimulate the olfactory system, essentially acting as physical therapy for the nose.