Other protracted symptoms of Covid-19 may also be explained by the inflammatory mechanism.
Covid-19 symptoms according to a group of scientists led by Duke Health:
The reason some people with Covid-19 fail to regain their sense of smell is related to an ongoing immune attack on olfactory nerve cells and a corresponding decline in the number of those cells.
The discovery offers a critical perspective on a frustrating issue that has plagued millions of people who have not fully regained their sense of smell following Covid-19.
The discovery sheds light on the potential biological mechanisms that may be responsible for other long Covid-19 symptoms, such as generalised fatigue, shortness of breath, and brain fog, in addition to the loss smell.
Loss of smell is frequently one of the first symptoms of Covid-19 infection, according to senior author Bradley Goldstein, an associate professor in Duke’s departments of head and neck surgery, communication sciences, and neurobiology.
Thankfully, a lot of people who experience altered smell during the acute phase of viral infection will regain smell within the next one to two weeks, but some do not, according to Goldstein.
“We need to learn more about why this subset of people will continue to experience persistent smell loss for months to years after contracting SARS-CoV2.”
In the study, which appeared online on December 21 in the journal Science Translational Medicine, Goldstein and colleagues from Duke, Harvard, and the University of California-San Diego
Examined olfactory epithelial samples taken from 24 biopsies, including nine patients who had long-term smell loss as a result of Covid-19.
The olfactory epithelium, the tissue in the nose that contains the smell nerve cells, was found to have a significant infiltration of T-cells engaged in an inflammatory response by this biopsy-based approach.
Which was used in collaboration with Sandeep Datta, M.D., Ph.D., at Harvard University.
Despite the absence of detectable SARS-CoV-2 levels, this particular inflammation process persisted.
Additionally, there were fewer olfactory sensory neurons, possibly as a result of ongoing inflammation damaging the sensitive tissue.
The results are startling, according to Goldstein. It almost seems like the nose is going through an autoimmune-like process.
According to Goldstein, identifying the damaged sites and the cell types involved is a crucial first step in developing treatments.
He claimed that the fact that neurons seemed to be able to repair themselves even after the protracted immune assault gave the researchers hope.
According to Goldstein, who noted that this work is currently being done in his lab
“We are hopeful that modulating the abnormal immune response or repair processes within the nose of these patients could help to at least partially restore a sense of smell.”
