Anosmia, or loss of sense of smell, is a well-known COVID-19 symptom – but less well-known is what actually causes it. However, a recent study may have finally uncovered part of the mystery of what goes on in our noses when we get COVID-19.
The virus doesn’t infect the neurons that detect odors, which makes sense given that SARS-CoV-2 infects less than 1 percent of cells in the human body. Instead, it attacks supporting cells that line the nasal cavity, the paper, published last month in Cell, found.
“Somehow, infections with SARS-CoV-2 can cause anosmia even though we know the virus enters only a very small percentage of the olfactory sensory neurons,” co-first author Dr Marianna Zazhytska said in a statement. “This indicates there is another way the virus is shutting down smell.”
It may not infect nerve cells directly, but SARS-CoV-2 still has an effect on them. After attacking and depleting adjacent cells, genetic changes are introduced in olfactory sensory neurons, altering their function. Chromosomal rearrangements in these neurons disrupt production of odor receptors – proteins that detect odor molecules in the nose – leading to loss of smell for between 30 and 75 percent of people with COVID-19 experience.
The damage is akin to a “collapsed house of cards”, co-first author Albana Kodra said.
Studies in golden hamsters revealed that, as well as a downregulation of odor receptors and related genes in sensory neurons, genes required for the sense of smell are also disrupted. The same was found when analyzing tissues from human autopsies.
“The nuclear architecture gets shattered in the sensory neurons even though it’s the [supporting] cells, not the neurons, that get infected,” Zazhytska said.
As for how this happens, the authors suggest that inflammation in supporting cells in response to infection could alter gene expression in the neighboring sensory neurons. The reorganization is not caused by the virus itself, but by the body’s immune response, Zazhytska told the New York Times.
Fortunately, the neurons don’t die, meaning the loss of smell is temporary – once the infection clears, the system can recover. However, this can take weeks, or even months.
The authors might not yet know the specific pathways and molecules involved, but they hope their work could one day help in understanding and diagnosing a whole host of diseases.
“Not only does this work reveal the mechanism underlying anosmia caused by COVID-19, but the findings could help us uncover relationships between olfaction and diseases, including Alzheimer’s and other neurodegenerative conditions,” co-author Dr Stavros Lomvardas said.
“We hope this new knowledge could lead to a better understanding, and maybe to diagnostic tools and treatments, for a number of conditions that involve damage to fragile nuclear architectures.”