The researchers found that the virus responsible for COVID-19 penetrates the nasal cavity via ACE2 receptor proteins which act as a gateway for the virus to penetrate human cells. Image: GrapeImages/IStock.com
According to a study by scientists at Harvard Medical School, the loss of smell in COVID-19 patients is likely to be caused by infection of nonneuronal cell types.
Loss of smell (or anosmia) is one of the most common symptoms of a COVID-19 infection, although it has not been clear what the mechanisms behind this phenomenon are. New research published in Science Advances by scientists at Harvard Medical School may provide the beginning of an explanation.
The authors of the paper focused on two existing theories around anosmia to attempt to understand where the symptom originates: in the cells of the mucus membranes of the nasal cavity or in the olfactory sensory neurons which send information to the brain.
They noted that the virus responsible for COVID-19 penetrates the nasal cavity via ACE2 receptor proteins which act as a gateway for the virus to penetrate human cells. This receptor protein is found in the cells furnishing metabolic and structural support to the olfactory sensory neurons, but not in olfactory sensory neurons themselves.
The discovery suggests that this symptom is more likely be caused by infection of the supporting cells, which in turn causes changes to the olfactory sensory neurons, rather than a neurological infection.
“Our findings indicate that the novel coronavirus changes the sense of smell in patients not by directly infecting neurons but by affecting the function of supporting cells,” said senior study author Sandeep Robert Datta, associate professor of neurobiology in the Blavatnik Institute at Harvard Medical School.
“I think it’s good news, because once the infection clears, olfactory neurons don’t appear to need to be replaced or rebuilt from scratch,” he said. “But we need more data and a better understanding of the underlying mechanisms to confirm this conclusion.” NVG
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