COVID-19 symptoms present as a diverse range of body aches, coughing, nausea, and more. For months, doctors have been trying to discover the cause of one of the virus’s most puzzling and lasting symptoms: loss of smell (or, “anosmia”). While researchers initially believed that the virus targeted and destroyed the nerves in the nasal passages that give your ability to stop and smell the roses, Harvard research published on July 28 presents an alternative theory that could be good news for the 17 million people worldwide who have contracted the virus.
Published in the journal Science Advances, the study sought to find the etiology—or the cause or series of causes—of the altered olfactory functioning sparked by the virus by looking at an existing database of cells. “We know that a lot of different viruses cause smell loss. And oftentimes, it can take many months for people’s sense of smell to come back after a rhinovirus or adenovirus or enterovirus,” explains Jessica Grayson, MD, an otolaryngologist and assistant professor at The University of Alabama Birmingham. ‘So researchers are using that information and looking at these people who are getting COVID Coronavirus.”
The fact that much of the population recovering from COVID-19 recovered their sense of smell back in weeks, not months, made scientists question if the virus actually damaged the nerves (which can recover, but on a much longer timeline, says Dr. Grayson). “We’ve always assumed that these coronaviruses attack the actual olfactory neurons, which are the smell neurons in the nose. They’re one of the few nerves that actually comes out of the brain and enter the nose,” says Dr. Grayson. “So what scientists were hypothesizing was: Maybe [the virus] is attacking something else.”
That hypothesis led researchers to consult a large database of olfactory cells taken from both humans and animals. They looked at the subjects’ ACE2 receptor, which is the receptor that scientists currently believe allow COVID to enter the cells. (The human body has an abundance of these types of receptors in the lungs—prompting the medical community to believe that it hits that organ the hardest.) “The researchers looked to see if olfactory neurons have ACE2 receptors and they didn’t. So they tested the cells around the olfactory neurons, which are called the supporting cells or sustentacular cells—which support the nerve with blood supply and provide the structure around it,” says Dr. Grayson. “And they found that those sustentacular cells actually do have an ACE2 receptor.” Meaning: The cells around the nerve (not the nerve itself) are taking the damage of the virus, which Dr. Grayson explains is really good news because cells heal much more rapidly than nerves. “Because those cells turn over very rapidly and regenerate very rapidly smell is coming back more quickly. Whereas, if the virus attacked a neuron or a nerve cell, those take much longer to regenerate. Months, sometimes a year,” she says.
The cells around the nerve (not the nerve itself) are taking the damage of the virus, which Dr. Grayson explains is really good news because cells heal much more rapidly than nerves.
Doctors now hope that what they’ve learned about the damage and the regeneration of the sustentacular cells will translate to the even more troubling neurological problems experienced by some COVID-19 patients. “Scientists think that maybe they’re also reversible with time because maybe it’s not affecting the actual nerve,” Dr. Grayson says. Of course, though, more research will have to be conducted before we can know that for sure.
Still, Dr. Grayson expresses that the virus’ influence on smell being temporary—not permanent—is a small scientific breakthrough that offers her some solace. Because, while we may not think about it on a daily basis the same way we do taste or vision, smell is a vital sense for our health and well-being. “If you can’t smell, you don’t know if your food is gone bad. You don’t know if your house is on fire. You do not know if your natural gas is leaking.”
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