Many COVID-19 patients experience anosmia—a complete loss of smell. After years of dedicated research, scientists have pinpointed the exact mechanism behind this distinctive symptom.
Anosmia involves a total loss of smell, which can be temporary or, rarely, permanent. It's common in respiratory infections like the flu or colds from milder coronaviruses, usually due to nasal congestion blocking aroma molecules from reaching olfactory receptors. Once congestion clears, smell typically returns.
COVID-19 changed that narrative. Early on, researchers suspected nervous system damage. Loss of smell and taste became hallmark symptoms, yet many patients lacked congestion. Even post-recovery, some reported prolonged anosmia. As noted in a June 24, 2020, The Conversation article, COVID-19-related anosmia stands apart from other infections.
These cases involve olfactory cleft syndrome, where swelling and mucus block the nose's odor-detection area, while sinuses and other regions remain clear—explaining the absence of a stuffy nose.
SARS-CoV-2 enters the body via ACE2 receptors on upper airway cells, aided by the TMPRSS2 protein, which facilitates viral invasion. Replication follows, sparking issues.
Initial theories suggested the virus directly infected and destroyed olfactory neurons. However, emerging research (including pre-prints) reveals ACE2 receptors are absent on these neurons' surfaces.
ACE2 receptors abound on "sustentacular" cells, which provide structural support for olfactory neurons. The virus targets these support cells, causing edema without neuron destruction. Post-recovery, swelling subsides, potentially restoring smell.
But severe cases involve intense inflammation—the body's immune response—which releases chemicals that can damage nearby tissues and cells. Here, olfactory neurons suffer indirect damage. Regeneration takes time, accounting for prolonged anosmia.
