The rationale some people fail to get better their sense of smell after COVID-19 is linked to an ongoing immune assault on olfactory nerve cells and an associated decline within the variety of those cells, a team of scientists led by Duke Health report.
The finding, publishing online Dec. 21 within the journal Science Translational Medicine, provides a crucial insight right into a vexing problem that has plagued tens of millions who haven’t fully recovered their sense of smell after COVID-19.
While specializing in 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 is likely to be triggered by similar biological mechanisms.
“Considered one of the primary symptoms that has typically been related to COVID-19 infection is lack of smell,” said senior creator Bradley Goldstein, M.D., Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology.
“Fortunately, many individuals who’ve an altered sense of smell in the course of the acute phase of viral infection will get better smell inside the subsequent one to 2 weeks, but some don’t,” Goldstein said. “We want to higher understand why this subset of individuals will go on to have persistent smell loss for months to years after being infected with SARS-CoV2.”
Within the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analyzed olfactory epithelial samples collected from 24 biopsies, including nine patients affected by long-term smell loss following COVID-19.
This biopsy-based approach — using sophisticated single-cell analyses in collaboration with Sandeep Datta, M.D., Ph.D., at Harvard University — revealed widespread infiltration of T-cells engaged in an inflammatory response within the olfactory epithelium, the tissue within the nose where smell nerve cells are situated. This unique inflammation process persevered despite the absence of detectable SARS-CoV-2 levels.
Moreover, the variety of olfactory sensory neurons were diminished, possibly resulting from damage of the fragile tissue from the continued inflammation.
The findings are striking. It’s almost resembling a form of autoimmune-like process within the nose.”
Bradley Goldstein, M.D., Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology
Goldstein said learning what sites are damaged and what cell types are involved is a key step toward starting to design treatments. He said the researchers were encouraged that neurons appeared to keep up some ability to repair even after the long-term immune onslaught.
“We’re hopeful that modulating the abnormal immune response or repair processes throughout the nose of those patients could help to a minimum of partially restore a way of smell,” Goldstein said, noting this work is currently underway in his lab.
He said the findings from this study could also inform additional research into other long-COVID-19 symptoms that is likely to be undergoing similar inflammatory processes.
Along with Goldstein and Datta, study authors include John B. Finlay, David H. Brann, Ralph Abi-Hachem, David W. Jang, Allison D. Oliva, Tiffany Ko, Rupali Gupta, Sebastian A. Wellford, E. Ashley Moseman, Sophie S. Jang, Carol H. Yan, Hiroaki Matusnami, and Tatsuya Tsukahara.
The study received funding support from the National Institutes of Health (DC018371, DC016859, AG074324, DC019956) and the Duke Department of Head and Neck Surgery & Communication Sciences.
Source:
Duke University Medical Center