Although the loss of smell and taste became clear symptoms of COVID-19 early in the pandemic, researchers are still investigating why that happens: Does the virus directly infect and destroy the cells responsible for these critical senses, or is it collateral damage through our immune system fighting off the invading enemy?
According to a postmortem study published this week in JAMA Neurology, it is the latter. The study — which delved deep into the noses, nerves and brains of 23 people who died from COVID-19 — is the most detailed look at the effects of the coronavirus on our sniffers. Researchers concluded that inflammation — not the virus — is behind the loss of smell and taste during a COVID-19 attack, which is good news in some ways. It suggests that treatments with anti-inflammatory drugs can prevent serious or long-term damage to those critical senses.
The finding follows a mix of data on the effects of SARS-CoV-2 on our sense of smell. Some data suggested that the virus may infect the nerves that carry smell signals to our brains — olfactory neurons. Thus, the lost senses can be caused by direct infections. But others found that the virus was not present in those neurons at death.
For the new study, researchers led by pathologist Cheng-Ying Ho of Johns Hopkins University examined the olfactory tissue of 23 patients who died from COVID-19 — nine of whom had lost all or part of their senses of smell and taste. Specifically, the researchers examined olfactory neurons in the nasal mucosa, blood vessels and the number of olfactory axons — which are parts of neurons that transmit electrical signals — in each patient. They also examined injuries to the olfactory bulb, the part of the brain where odor signals are received, and determined whether SARS-CoV-2 was present or not.
They compared the findings with those of 14 people who died of other causes and were not infected with COVID-19 and had no loss of smell or taste.
Follow the scent
Compared to controls and COVID-19 patients without altered smell and taste, the COVID-19 patients with altered senses of smell and taste had more injuries to their nasal mucosa, more damage to their vasculature and significantly fewer olfactory axons.
However, that damage to the olfactory tissue was not linked to the documented severity of the patients’ COVID-19 infections — for example, some people with mild COVID-19 infections had severe injuries to their olfactory bulbs. In addition, only three of the 23 patients had detectable levels of SARS-CoV-2 genetic material in their olfactory bulb. Of those three, only one had reported loss of smell. The other two reported no loss of taste or smell. These results suggest that “olfactory pathology was not caused by direct viral damage,” the authors concluded.
“Previous studies based only on routine pathological examinations of tissue — and not the in-depth and ultra-fine analyzes we performed — suspected that viral infection of the olfactory neurons and the olfactory bulb might play a role in the loss of smell associated with COVID -19,” Ho said in a statement. “But our findings suggest that SARS-CoV-2 infection of the olfactory epithelium leads to inflammation, which in turn damages neurons, reduces the number of axons available to send signals to the brain and causes the olfactory bulb to become dysfunctional.”
This dysfunction can be so severe that loss of smell and taste can last for a long time or cause permanent damage. But, Ho noted in an audio interview, “if inflammation is the main cause of the injury in olfactory structures, it’s possible we could use anti-inflammatory drugs as a treatment,” she said. “That’s what I hope our study can inspire — future studies to explore this.”
