Long COVID, found the reason for the loss of smell.
An immune mechanism could contribute to the long-term loss of smell, but it could also explain other symptoms of COVID-19.
The reason some people fail to recover their sense of smell after COVID-19 is linked to an ongoing immune attack on olfactory nerve cells and a decrease in the number of nerve cells themselves, according to a team of scientists led by Duke Health. The finding, published in the journal Science Translational Medicine, provides important insight into a nagging problem that has plagued millions of people who have not fully recovered their sense of smell after COVID-19.
While focusing on the loss of smell, the finding also sheds light on possible underlying causes of other long COVID symptoms – including generalized fatigue, shortness of breath and brain fog – that could be triggered by similar biological mechanisms.
“One of the early symptoms typically associated with COVID-19 infection is loss of smell,” said lead author Bradley Goldstein, an associate professor in the Department of Head and Neck Surgery and Communication Sciences at Duke and the University of California. Department of Neurobiology.
“Fortunately, many people who have a smell impairment during the acute phase of the viral infection recover their sense of smell within a week or two, but some do not,” Goldstein said. “We need to better understand why this subset of people continue to have a persistent loss of smell for months to years after SARS-CoV2 infection.”
In the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analyzed samples of olfactory epithelium collected from 24 biopsies, including those from nine patients with long-term loss of smell following COVID-19. This biopsy-based approach – using sophisticated single-cell analysis – revealed widespread infiltration of T lymphocytes engaged in the inflammatory response into the olfactory epithelium, the tissue in the nose where the nerve cells for smell are found. This unique inflammatory process persisted despite the absence of detectable levels of SARS-CoV-2.
In addition, the number of olfactory sensory neurons decreased, perhaps due to damage to delicate tissue from ongoing inflammation.
“The results are amazing,” Goldstein said. “It almost looks like some sort of autoimmune process in the nose.”
Goldstein said knowing which sites are damaged and which cell types are involved is a critical step in starting to design treatments.
“We hope that modulating the abnormal immune response or repair processes within the noses of these patients could help restore at least some sense of smell,” Goldstein said, noting that this work is currently ongoing in his studio. laboratory. Goldstein added that the findings of this study could also be useful for further research into other long-lasting symptoms of COVID-19 that may be prone to similar inflammatory processes.