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Prolonged Sense of Smell after COVID-19 Attributed to Persistent Immune Assaults

A new study shows that those whose sense of smell never returned after COVID-19 are under constant immune attacks

Holden Galusha

Holden Galusha is the associate editor for Lab Manager. He was a freelance contributing writer for Lab Manager before being invited to join the team full-time. Previously, he was the...

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Researchers from the Duke University Medical Center have uncovered the reason that some people who catch COVID-19 fail to recover their sense of smell afterward: an ongoing immune assault on olfactory nerve cells, which leads to a decline in the number of those cells. Armed with this new information, researchers may be able to devise a way to modulate the immune response of these patients to improve their sense of smell.

One of the first symptoms of COVID-19 is the loss of smell. For many, the symptom is temporary, lasting only for the duration of the infection’s acute phase. But for millions, that sense never returned, even long after the infection. “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-CoV-2,” said senior author Bradley Goldstein, MD, PhD, associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology.

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Goldstein and his research team took the study, published in Science Translational Medicinein a  “biopsy-based approach,” according to a news release from Duke Health. The team analyzed samples of olfactory epithelial tissue from 24 patients, nine of whom had long-term loss of smell as a result of past COVID-19 infections. They found that in all nine patients experiencing smell loss, there was a “widespread infiltration of T-cells engaged in an inflammatory response in the olfactory epithelium,” or the nose tissue where smell nerve cells are located. This inflammation persisted in the patients even though COVID-19 was not detected in the patients’ bodies. The overall number of olfactory sensory neurons were reduced as well, which the researchers hypothesize was caused by damage to the tissue from persistent inflammation. “The findings are striking. It’s almost resembling a sort of autoimmune-like process in the nose,” Goldstein said.

According to Goldstein, learning where the damage is and what types of cells are involved is key to designing treatments for prolonged smell loss. Goldstein and his team believe that developing techniques to modulate both the immune response and the sensory neuron’s repair processes could pave the way to at least partially restoring patients’ senses of smell. This work is now underway in Goldstein’s laboratory.