It has happened to millions during the pandemic: a sudden loss of smell that heralds the start of a COVID-19 infection. But scientists have been stumped as to why.
New research suggests the symptom is due to inflammation rather than directly caused by the coronavirus.
The researchers noted that loss of smell (anosmia) is a common and often long-term symptom of COVID-19 that can have a serious impact on a person’s quality of life because it can reduce the ability to taste, make it difficult to detect airborne warnings of danger and affect other aspects of daily life.
“As a neuropathologist, I wondered why smell loss is a very common symptom with COVID-19 but not with other respiratory diseases,” said study lead author Dr. Cheng-Ying Ho. She is an associate professor of pathology at Johns Hopkins University School of Medicine, in Baltimore.
“So, we decided to dig deeply into the mechanics of smell, to see what actually occurs at the cellular level when SARS-CoV-2 invades the body,” Ho said in a university news release.
The investigators analyzed tissues from the olfactory bulb at the base of the brain — a region that transmits nerve impulses carrying information about odors — from 23 people who died from COVID-19 and a control group of 14 who died from other causes and who had no detectable coronavirus at the time of their deaths.
Three of the 23 patients with COVID-19 had lost their sense of smell, four had reduced smell and two had loss of both smell and taste. None of the 14 patients in the control group had lost either smell or taste.
“When we compared the tissues from patients without COVID-19 with those from persons who had been infected with SARS-CoV-2 — especially the ones with diminished or complete loss of smell — we found that the group with COVID showed more severe vascular injury and far fewer axons [portions of neurons that transmit electrical impulses] in the olfactory bulb,” Ho said.
“And that didn’t change when we statistically controlled for the impact of age, strongly suggesting that these effects aren’t age-related and, therefore, are linked to SARS-CoV-2 infection,” she explained.
However, Ho said the team was surprised to find that despite nerve and vascular damage, SARS-CoV-2 particles were not detected in the olfactory bulb in the majority of patients with COVID-19.
“Previous investigations that only relied on routine pathological examinations of tissue — and not the in-depth and ultra-fine analyses we conducted — surmised that viral infection of the olfactory neurons and olfactory bulb might play a role in loss of smell associated with COVID-19,” Ho noted.
“But our findings suggest that SARS-CoV-2 infection of the olfactory epithelium leads to inflammation, which in turn, damages the neurons, reduces the numbers of axons available to send signals to the brain and results in the olfactory bulb becoming dysfunctional,” she concluded
The study was published online recently in JAMA Neurology.
The next step is to compare tissues from patients who died of the Delta and Omicron variants of the coronavirus.
“We want to compare any axon damage and bulb dysfunction found in those tissues with what we observed in patients who had the original virus strain,” Ho said. “That way, we’ll be able to better predict if Delta and Omicron are more or less likely to cause loss of smell.”
For more on COVID-19 and loss of smell, go to the U.K.’s National Health Service.
SOURCE: Johns Hopkins Medicine, news release, April 11, 2022