Although the loss of smell and taste became obvious symptoms of COVID-19 early in the pandemic, researchers are still working on why this happens — does the virus directly infect and destroy the cells responsible for these critical senses, or is it collateral damage from our immune system fighting off the invading enemy?
Corresponding a postmortem study coming out 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 impact of the coronavirus on our snoopers. The researchers concluded that inflammation — not the virus — is behind the loss of smell and taste during a bout of COVID-19, which is good news in some ways. It suggests that anti-inflammatory drug treatments could prevent serious or long-term damage to these 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 can infect the nerves that carry smell signals to our brain – olfactory neurons. So the lost senses could be caused by direct infections. But others found that the virus was not present in these neurons at death.
For the new study, researchers led by Johns Hopkins University pathologist Cheng-Ying Ho examined the olfactory tissue of 23 patients who died from COVID-19 – nine of whom had lost all or part of their sense of smell and taste. Specifically, the researchers looked at olfactory neurons in the nasal lining, blood vessels, and the number of olfactory axons — which are parts of neurons that transmit electrical signals — in each patient. They also looked at injuries to the olfactory bulb, the part of the brain where olfactory signals are received, and determined whether or not SARS-CoV-2 was present.
They compared the results to those of 14 people who died from 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 With altered senses of 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 vascular system, and significantly fewer olfactory axons.
However, this damage to the olfactory tissue was not linked to the documented severity of the patients’ COVID-19 infection – some people with mild COVID-19 infections, for example, had severe injuries to their olfactory bulb. In addition, only three of the 23 patients had detectable levels of SARS-CoV-2 genetic material in their olfactory bulbs. Of those three, only one had reported a loss of smell. The other two reported no loss of taste or smell. These results suggest that “the olfactory pathology was not caused by direct viral injury,” the authors concluded.
“Previous research, based only on routine pathological tissue examinations – and not on the detailed and ultrafine analyzes we performed – suggested that viral infection of the olfactory neurons and olfactory bulb could play a role in smell loss associated with COVID-19 . said Ho a statement. “But our results suggest that SARS-CoV-2 infection of the olfactory epithelium leads to inflammation, which in turn damages the neurons, reducing the number of axons available to send signals to the brain and leading to dysfunction of the olfactory epithelium olfactory bulb.”
This dysfunction can be so severe that loss of smell and taste can last for long periods or cause permanent damage. But, Ho in remarked an audio interview, “If inflammation is the primary cause of injury to the olfactory structures, it’s possible we can use anti-inflammatory agents to treat it,” she said. “That’s what I hope our study can inspire — future studies to look at.”
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