COVID-19 causes smell and taste loss by attacking the support cells inside your nose, not the nerve cells themselves. The virus latches onto a specific receptor found on these support cells, disrupting the delicate system that lets you detect odors. This was one of the most distinctive symptoms of the pandemic, affecting roughly 40% of people infected with earlier variants, though that number has dropped significantly with Omicron.
How the Virus Disrupts Your Sense of Smell
The inside of your nose is lined with a thin tissue called the olfactory epithelium. This tissue contains two key cell types: sensory neurons that detect odors and send signals to your brain, and sustentacular cells that act as support staff, keeping those neurons healthy and functional. Sustentacular cells provide structural support, regulate the chemical environment around the neurons, and help process odor molecules so neurons can detect them.
SARS-CoV-2 targets sustentacular cells because they carry high levels of a receptor called ACE2 on their surface, along with a protein called TMPRSS2 that helps the virus get inside. The sensory neurons themselves don’t carry these receptors, which is actually good news: the virus isn’t directly destroying the cells responsible for smell. Instead, it’s knocking out their support system. When sustentacular cells become infected and inflamed, the signaling pathways that neurons rely on to detect and transmit odor information get disrupted. The result is a sudden, often complete loss of smell.
Imaging studies of infected patients point to inflammation concentrated at the level of this nasal tissue rather than deeper in the brain. Some patients have shown temporary swelling of the olfactory bulb, the brain structure that receives signals from the nose, but the primary damage happens locally in the nasal lining.
Why You Seem to Lose Taste Too
Most people who report losing their sense of taste during COVID are actually experiencing something different from what they think. True taste, the ability to detect sweet, salty, sour, bitter, and umami, relies on taste buds on your tongue. But the rich experience of flavor comes largely from smell. When you chew food, volatile compounds travel from the back of your mouth up into your nasal cavity, a process called retronasal olfaction. This is why food tastes “like nothing” when you have a bad cold.
With COVID, the same thing happens on a more dramatic scale. When the virus wipes out your ability to smell, food loses most of its complexity, and your brain interprets that as losing taste. Some research suggests the virus may also directly affect taste bud cells, but objective testing of true taste function in COVID patients is still limited. For most people, what feels like taste loss is really smell loss in disguise.
Earlier Variants Hit Harder Than Omicron
Smell loss was practically a hallmark of early COVID strains. Meta-analyses covering the first year of the pandemic found that around 38 to 43% of patients reported olfactory problems. That changed dramatically with Omicron. A systematic review found that Omicron’s effect on smell is two to tenfold lower than earlier variants like Alpha or Delta. The global prevalence of Omicron-related smell loss in adults is estimated at just 3.7% when adjusted for population size and ethnic differences.
There’s also a notable genetic and ethnic component. Among populations of European ancestry, Omicron-induced smell loss runs around 11.7%, while other populations range between 1.9% and 4.9%. This likely reflects differences in the genes that code for the ACE2 receptor and related proteins in nasal tissue.
Distorted Smells During Recovery
For some people, getting their smell back isn’t a clean return to normal. Instead, they go through a phase where familiar scents smell wrong or unpleasant, a condition called parosmia. Coffee might smell like garbage. Meat might smell chemical or rotten. Others experience phantom smells, detecting odors that aren’t there at all.
These distortions are thought to occur because the olfactory neurons are regenerating and rewiring. As new neurons grow and reconnect with the brain, the signals can get scrambled. In one study tracking COVID patients over time, about 9% of participants who had fully recovered their smell after 100 days later developed new distortions months after the initial infection. These qualitative changes can persist for several months, and their onset can be delayed well beyond the acute illness.
Why Some People Don’t Recover
Most people regain their sense of smell within weeks or a few months. But a subset of patients experience persistent loss that lasts a year or more. Research published through the RECOVER COVID initiative, which involved biopsies of the nasal tissue in people with long-term smell loss, found something striking: the virus itself was long gone, with no detectable viral RNA or protein remaining in the tissue. But the immune system hadn’t stood down.
The biopsies revealed a persistent infiltration of T cells producing inflammatory signals, along with shifts in other immune cell populations. Anti-inflammatory immune cells were depleted, while certain inflammatory cell types were enriched. This ongoing immune response appeared to be affecting the sustentacular cells, which showed gene expression patterns consistent with reacting to chronic inflammation. Critically, the number of olfactory sensory neurons was reduced relative to the support cells, suggesting the inflammatory environment was preventing full neuronal regeneration.
In plain terms, the lingering inflammation in the nose, not residual virus or permanent nerve damage, appears to be what keeps some people from recovering their sense of smell. The tissue is stuck in a cycle of immune activation that disrupts the environment neurons need to function and replenish themselves.
Smell Training as a Recovery Tool
The most widely recommended rehabilitation approach is olfactory training, a structured daily practice of sniffing specific strong scents. Protocols used in clinical settings typically involve smelling a rotation of distinct odors every day for at least two months. Common choices include vanilla, coffee, cinnamon, cloves, lavender, mint, and thyme, chosen because they activate different types of smell receptors.
The idea behind smell training is similar to physical therapy after an injury: repeated, deliberate stimulation encourages the regenerating neurons to form correct connections with the brain. Clinical trials are still evaluating exactly how effective this approach is, and results vary from person to person. But it’s low-risk, costs almost nothing, and is supported by decades of use in treating smell loss from other causes like head injuries and viral infections that predate COVID.
If you want to try it at home, the standard approach is to hold each scent a few inches from your nose and inhale gently for 15 to 20 seconds, focusing on trying to identify and remember the smell. Do this with four to five different scents, twice a day. Consistency matters more than intensity.
How Smell Loss Is Measured Clinically
If smell loss persists, doctors can measure it objectively using standardized scratch-and-sniff tests. The most widely used is the University of Pennsylvania Smell Identification Test, or UPSIT, which presents 40 unique odors that you scratch, sniff, and try to identify from multiple-choice options. Your score is then compared against norms for your age and sex. This kind of testing is more reliable than self-reporting, since many people overestimate or underestimate their own smell ability. The RECOVER COVID study used this test on participants roughly two years after infection to track long-term olfactory outcomes.