An ongoing immune assault on olfactory nerve cells and an associated decline in the number of those cells may explain why some people fail to recover their sense of smell after COVID-19.
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 COVID-19.
While focusing on the loss smell, the finding also sheds light on the possible underlying causes of other long COVID-19 symptoms—including generalized fatigue, shortness of breath, and brain fog—that similar biological mechanism might trigger.
“One of the first symptoms that has typically been associated with COVID-19 infection is loss of smell,” says senior author Bradley Goldstein, associate professor in the head and neck surgery and communication sciences department and the neurobiology department at Duke University.
“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 SARS-CoV2.”
In the study, Goldstein and colleagues analyzed olfactory epithelial samples collected from 24 biopsies, including nine patients suffering from long-term smell loss following COVID-19.
This biopsy-based approach—using sophisticated single-cell analyses in collaboration with Sandeep Datta of Harvard University—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 unique inflammation process persisted despite the absence of detectable SARS-CoV-2 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,” Goldstein says. “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 says the researchers were encouraged that neurons appeared to maintain some ability to repair even after the long-term immune onslaught.
“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,” Goldstein says, noting this work is currently underway in his lab.
He says the findings from the study could also inform additional research into other long-COVID-19 symptoms that might be undergoing similar inflammatory processes.
Additional coauthors are from the University of California, San Diego; Harvard University; and Duke. The National Institutes of Health and the Duke Department of Head and Neck Surgery & Communication Sciences funded the work.
Source: Duke University
