During the pandemic, millions of people experienced a sudden loss of smell, which signaled the start of a COVID-19 infection. However, scientists are baffled as to why.
According to new studies and US News, the illness is caused by inflammation rather than the coronavirus.
Loss of smell (anosmia) is a prevalent and often long-term symptom of COVID-19 that can have a significant influence on a person’s quality of life since it impairs taste, makes it challenging to detect airborne indications of danger, and affects other elements of everyday living, according to the study.
“As a neuropathologist, I’ve always wondered why smell loss is so widespread in COVID-19 but not in other respiratory disorders,” said Dr. Cheng-Ying Ho, the study’s primary author. She works as an associate professor of pathology at Baltimore’s Johns Hopkins University School of Medicine.
“So we decided to go into the mechanics of scent to see what happens at the cellular level when SARS-CoV-2 infects the body,” Ho stated in a university press statement.
The researchers compared samples from 23 patients who died from COVID-19 to a control group of 14 persons who died from other causes and had no detectable coronavirus.
Three of the 23 COVID-19 patients had lost their sense of smell, four had reduced sense of smell, and two had both smell and taste loss. The 14 patients in the control group had neither lost their scent nor their taste.
“We found that the group with COVID had a more severe vascular injury and far fewer axons [portions of neurons that transmit electrical impulses] in the olfactory bulb when we compared tissues from patients without COVID-19 with those from people who had been infected with SARS-CoV-2 — especially those with diminished or complete loss of smell,” Ho said.
“And that didn’t change when we statistically controlled for the effect of age,” she explained, “strongly suggesting that these effects aren’t age-related and, thus, are linked to SARS-CoV-2 infection.”
Despite nerve and vascular damage, Ho said the team was shocked to find that SARS-CoV-2 particles were not detected in the olfactory bulb in most COVID-19 patients.
“Previous studies that relied solely on standard pathological examinations of tissue — rather than the in-depth and ultra-fine analysis we performed,” Ho explained, “suggested that viral infection of the olfactory neurons and olfactory bulb might play a role in COVID-19-related loss of smell.”
“However, our findings show that SARS-CoV-2 infection of the olfactory epithelium causes inflammation, which destroys neurons, lowers the number of axons available to relay signals to the brain, and leads to olfactory bulb dysfunction,” she concluded.
JAMA Neurology has published the study online.
The next stage compares tissues from individuals who died from coronavirus variants Delta and Omicron.
“Any axon damage and bulb malfunction discovered in those tissues will be compared to what we saw in patients with the initial viral strain,” Ho explained. “By doing so, we’ll be able to forecast whether Delta and Omicron are more or less likely to induce odor loss.”