Inflammation, not coronavirus, may be behind loss of smell: Johns Hopkins

Loss of smell from COVID-19 may be a consequence of inflammation caused by the infection, versus a direct outcome from the virus itself, according to a study published April 11 in JAMA Neurology.

A team led by researchers at Baltimore-based Johns Hopkins Medicine analyzed brain tissue samples taken from the olfactory bulb of 23 people who died of COVID-19 and 14 who died of other causes. Three of the 23 people with COVID-19 lost their sense of smell, four lost some ability to smell and two lost both their sense of smell and taste.

People with COVID-19 had more severe vascular injury and fewer axons in the olfactory bulb, the part of the brain responsible for transmitting neural input about odors. This trend was consistent even after researchers controlled for age.

While researchers found more nerve and vascular damage among people with COVID-19, most of their tissue samples did not contain SARS-CoV-2 virus particles. 

"Previous investigations that only relied on routine pathological examinations of tissue — and not the in-depth and ultrafine 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," lead author Cheng-Ying Ho, MD, PhD, associate professor of pathology at Johns Hopkins University School of Medicine, said in a news release. "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."

View the full study here.

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