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Scientists find key reason why loss of smell occurs in long covid

long covid

Durham, US – The reason some people fail to recover their sense of smell after covid is linked to an ongoing immune assault on olfactory nerve cells and an associated decline in the number of those cells, scientists from Duke University in the US say.

The finding, published in the journal Science Translational Medicine, provides an important insight into a vexing problem that has plagued millions who have not fully recovered their sense of smell after getting covid. The inflammatory mechanism could also help explain other long covid symptoms.

While focusing on the loss smell, the finding also sheds light on the possible underlying causes of other long covid issues including fatigue, shortness of breath and brain fog that might be triggered by similar biological mechanisms.

One of the first symptoms that has typically been associated with covid is loss of smell, says scientist Dr Bradley Goldstein, associate professor in Duke’s department of head and neck surgery and communication sciences and the department of neurobiology.

“Fortunately, many people who have an altered sense of smell during the acute phase of viral infection will recover smell within the next one to two weeks, but some do not,” Goldstein says.

“We need to better understand why this subset of people will go on to have persistent smell loss for months to years after being infected with covid.”

In the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analysed olfactory epithelial samples collected from 24 biopsies, including nine patients suffering from long-term smell loss following COVID-19.

This biopsy research, using sophisticated single-cell analyses revealed widespread infiltration of T-cells engaged in an inflammatory response in the olfactory epithelium, the tissue in the nose where smell nerve cells are located.

This inflammation process persisted despite the absence of detectable covid levels. Additionally, the number of olfactory sensory neurons were diminished, possibly due to damage of the delicate tissue from the ongoing inflammation.

The findings are striking. It’s almost resembling a sort of autoimmune-like process in the nose.

Goldstein says learning what sites are damaged and what cell types are involved is a key step toward beginning to design treatments. He said the researchers were encouraged that neurons appeared to maintain some ability to repair even after the long-term immune onslaught.

The scientists are hopeful that modulating the abnormal immune response or repair processes within the nose of these patients could help to restore a sense of smell at least partially.

The findings from the study could inform additional research into other long-covid symptoms that might be undergoing similar inflammatory processes.