New research, published in the journal Science Translational Medicine, may have identified why some individuals suffering from long COVID-19 fail to recover their sense of smell.
Anosmia, or loss of smell, is a common symptom for those suffering from COVID-19, but in most cases this sense returns soon after recovery from the infection. However for some people, anosmia can continue to persist even years afterwards.
Now, new information has shown that this ongoing loss of smell could be due to COVID-induced immune attack and loss of cells in the area controlling this sense.
As part of their work, the team analysed olfactory epithelial samples taken from 24 biopsies, of which nine were taken from individuals suffering from ongoing loss of smell following COVID-19 infection. The olfactory epithelium is part of the nasal cavity where the olfactory sensor neurons are found – nerve cells which allow the perception of smell.
Controls for the experiments included samples from individuals with no history of COVID-19 and those with a previous diagnosis of COVID-19, where sense of smell was reported as normal.
When the team initially compared the hyposmic samples (belonging to those with loss of smell) to the normosmic controls (from those with a normal sense of smell), they found that the hyposmic samples contained a higher number of T cells, a critical component of the immune system.
On taking a closer look at the specific types of T cells expressed in the hyposmic samples, they found a unique sub-type which produces interferon-gamma, a pro-inflammatory molecule which stimulates the immune system into action.
There was also an increase in the quantity of CD207+ dendritic cells, which are able to control the activation of T cells.
Interestingly, the team found that there was a decrease in the amount of M2 macrophages found in the hyposmic samples. These cells are anti-inflammatory and are involved in the repair of damaged tissue.
When the team analysed sustentacular cells in the samples (cells found in the olfactory epithelium which support the sensory neurons), they identified that gene expression in the hyposmic samples was markedly altered, consistent with a response to inflammation, versus the controls.
Finally, they were also able to demonstrate that in the hyposmic samples, there was a reduction in the number of the olfactory sensory neurons, potentially because of the increased presence and action of T cells and the damage caused by inflammation.
“These findings are striking,” says Bradley Goldstein, MD, PhD, a primary author of the paper and Associate Professor in the Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology at Duke University School of Medicine. “It’s almost resembling a sort of auto-immune-like process in the nose”.
By starting to understand the reasons behind ongoing anosmia in long COVID-19, we can be in a better position to begin planning for treatments to alleviate this troubling condition, such as by specifically blocking the action of pro-inflammatory cells. The paper explains that the site of the olfactory epithelium means that a localised topical delivery of the drug, where the medicine could be directly applied in the naval cavity, may be a possibility.
“We are hopeful that modulating the abnormal immune response or repair processes within the nose of the patient could help to at least partially restore a sense of smell,” Goldstein continued.
The paper can found found here.