Anosmia, the loss of one’s sense of smell, is common during COVID-19 and can persist for months or years after acute infection for reasons that have remained unclear. Research led by Duke University School of Medicine has now shed more light on this perplexing problem that continues to vex millions. Learn what they discovered about what causes anosmia.*

Current thought on COVID-related loss of smell

In the journal Science Translational Medicine, the researchers explain that loss of smell after severe COVID-19 is believed to be due to the virus’ impact on the epithelium cell layer that lines the upper nasal passages. Epithelial tissue contains sensory neurons that allow us to smell (olfaction). While changes in these neurons and inflammation are thought to cause acute loss of smell in animal studies of COVID infection, other research on humans and animals has shown that supporting (sustentacular) cells of the epithelium are the main infection site. 

It’s believed that, after the virus has cleared, these supporting cells and any damaged neurons are repaired and smell is restored. We still aren’t clear, however, why loss of smell only persists in certain people after acute infection. Autopsies of people who died from COVID-19 have shown:

• Persistent infection of supporting cells,
• No infection of sensory neurons with intact epithelium, and
• Diverse changes in sensory neurons that could lead to loss of smell.

Though these findings point to causes of acute loss of smell from COVID-19, the researchers say that direct analysis of tissue from people currently living with anosmia is lacking.

What the researchers did

The Duke team collected human samples of olfactory epithelium from 24 biopsies, including nine (9) people with chronic loss of smell after COVID.

• Samples were examined for cellular and genetic changes associated with loss of smell from COVID.
• Results were compared to control samples of normal-functioning epithelial and mucosal nasal tissue.

What they found

The team members found that:

• Compared to controls, there was extensive inflammation in nose epithelium by widespread T-cell (white blood cell) infiltration, despite no detectable COVID virus. 
• There were reduced levels of sensory neurons, possibly from cellular damage caused by ongoing inflammation.

According to the researchers, genetic differences in dysfunctional nasal epithelium versus normal tissue suggest post-COVID immune-driven changes in supporting cells and sensory neuron function.

“The findings are striking,” said senior study author Bradley Goldstein, M.D., Ph.D. “It’s almost resembling a sort of autoimmune-like process in the nose.”

What it means

Goldstein explains that knowing which nasal sites are damaged from COVID infection, and the cell types involved, is a critical initial step in designing treatments. He says the researchers are encouraged to find that, even after long-term inflammation, sensory neurons seem to maintain some capacity for repair.

“We are hopeful that modulating the abnormal immune response or repair processes within the nose of these patients could help to at least partially restore a sense of smell,” he said, adding that the findings could also shed light on the mechanics of other Long COVID symptoms.

*Duke University Medical Center. (2022, December 22). Scientists find key reason why loss of smell occurs in long COVID-19. MDLinx. https://www.mdlinx.com/news/scientists-find-key-reason-why-loss-of-smell-occurs-in-long-covid-19