Study sheds light on why some people have persistent loss of smell after COVID-19 infection.
The reason why some people fail to regain their sense of smell after infection with COVID-19 is linked to an ongoing immune attack on olfactory nerve cells and an associated decrease in the number of these cells, reports a team of scientists led by Duke Health.
The discovery, published online Dec. 21 in the journal Science Translational Medicineprovides important insight into an upsetting issue for millions of people who haven’t fully recovered their sense of smell after the COVID-19 operation.
While focusing on the loss of sense of smell, this finding also sheds light on the possible underlying causes of other longstanding symptoms of COVID-19 — including generalized fatigue, shortness of breath and brain fog — that could be triggered by similar biological mechanisms.
“One of the first symptoms commonly associated with COVID-19 infection is loss of sense of smell,” said lead author Bradley Goldstein, MD, Ph.D., associate professor in the Department of Surgery at Head and Neck and Communication Sciences and in the Department of Neurobiology at Duke.
“Fortunately, many people whose sense of smell is impaired during the acute phase of a viral infection recover their sense of smell within the next week or two, but some do not recover it,” Goldstein said. “We need to better understand why this subset of people will exhibit persistent loss of smell for months or even years after being infected with SARS-CoV2. »
In the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analyzed samples of olfactory epithelium taken from 24 biopsies, including nine patients with long-term loss of smell. following COVID-19.
This biopsy-based approach — using sophisticated single-cell analyzes in collaboration with Sandeep Datta, MD, Ph.D., of Harvard University — revealed extensive infiltration of T cells engaged in an inflammatory response in the olfactory epithelium, the tissue of the nose where the nerve cells of smell are located. This unique inflammatory process persisted despite the absence of detectable levels of SARS-CoV-2.
Additionally, the number of olfactory sensory neurons decreased, likely due to damage to delicate tissue from ongoing inflammation.
The results are striking. It almost sounds like some kind of autoimmune process in the nose. »
Bradley Goldstein, MD, Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and Department of Neurobiology.
Goldstein said learning which sites are damaged and which cell types are involved is a key step to start designing treatments. He added that the researchers were encouraged that the neurons seemed to retain some capacity for repair even after a long-lasting immune assault.
“We hope that modulating the abnormal immune response or repair processes in the noses of these patients could help restore at least a partial sense of smell,” Goldstein said, noting that this work is currently underway. in his laboratory.
He added that the results of this study could also serve as a basis for further research into other symptoms of COVID-19 infection that may undergo similar inflammatory processes.
Besides Goldstein and Datta, the authors of the study are 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.
This study received financial support from the National Institutes of Health (DC018371, DC016859, AG074324, DC019956) and the Duke Department of Head and Neck Surgery & Communication Sciences.
Duke University Medical Center
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