Autopsies suggest smell loss from COVID is caused by inflammation, not a virus

Enlarge / A woman holds a nasal swab for a rapid COVID-19 antigen test outside her office on January 5 in Berlin.

Although loss of smell and taste became an apparent symptom of COVID-19 early in the pandemic, researchers are still trying to determine why this is happening: does the virus directly infect and destroy cells responsible for these critical senses, or is it collateral damage of our immune systems fighting off the invading enemy?

According to a post-mortem study published this week in JAMA Neurology, this is the latest. The study – which delved deep into the noses, nerves and brains of 23 people who died of COVID-19 – is the most detailed examination of the effects of the coronavirus on our sniffers. The researchers concluded that inflammation — not the virus — is to blame for the loss of smell and taste during an episode of COVID-19, which is good news in some ways. This suggests that treatments with anti-inflammatory drugs 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 suggests that the virus can infect the nerves that transmit olfactory signals to our brain, the olfactory neurons. Thus, the lost senses could be caused by direct infections. But others have found that the virus was not present in these neurons at the time of death.

For the new study, researchers led by Johns Hopkins University pathologist Cheng-Ying Ho closely examined the olfactory tissues of 23 patients who died with COVID-19, nine of whom had completely or partially lost their sense of smell and taste. . Specifically, the researchers looked at 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 looked at lesions in 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 of other causes and who were not infected with COVID-19 and had no loss of smell or taste.

Following the smell

Compared to controls and COVID-19 patients without altered smell and taste, COVID-19 patients who had impaired senses of smell and taste had more injury to the nasal mucosa, more damage to their vasculature, and significantly fewer olfactory axons.

However, this damage to olfactory tissue was unrelated to the documented severity of patients’ COVID-19 infections — some people who had mild COVID-19 infections had severe injuries to their olfactory bulbs, for example. Additionally, only three of the 23 patients had detectable levels of SARS-CoV-2 genetic material present in their olfactory bulbs. Of these 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 investigations that relied only on routine pathological examinations of tissues—and not on the in-depth, ultra-thin analyzes we conducted—have speculated that viral infection of olfactory neurons and the olfactory bulb may 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 the neurons, reduces the number of axons available to send signals to the brain and leads to dysfunction of the olfactory bulb.”

This dysfunction can be so severe that the loss of smell and taste can persist for long periods of time or cause permanent damage. But, Ho noted in an audio interview, “if inflammation is the primary cause of injury in olfactory structures, it’s possible we could use an anti-inflammatory agent as a treatment,” she said. “That’s what I hope our study can inspire – future studies to look at this.”

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