The international group of scholars from Belgium and the United States explained the true mechanism for the loss of sense of smell under COVID-19. Researchers failed to find evidence that the infection affects the sensory neurons of the olfactory epithelium or the cells is the nervous olfactory bulbs. Thus, the coronavirus is not a neurotropic virus, but SARS-COV-2 affects another type of cells in the sense of smell. This is reported in an article published in Cell magazine.
When infected with SARS-COV-2, the Ace2 receptor on the cell membrane is associated with the ACE2 receptor. This receptor is expressed on the surface of crustacular cells, but not in olfactory sensory neurons, which transmit signals about smelling into an olfactory bulb. Sustacular cells provide neurons with nutrients and maintain their structure. Both types of cells are continuously regenerated from stem cells of an olfactory epithelium throughout the human life.
Researchers analyzed the samples of the olfactory nasal mucosa in the died of COVID-19 patients. As a control, samples of tissues in patients who died and for other reasons were not infected with SARS-COV-2 were taken. The tissue of the mucous membrane and samples of the olfactory bulbs were obtained using endoscopes for 60-90 minutes after death.
Results show that SARS-COV-2 infects crustacular cells in the olfactory epithelium of patients with COVID-19 and is actively replicated in these cells. However, viral RNA failed to detect in sensory neurons and neurons of the olfactory bulb. According to scientists, the cause of temporary olfactory dysfunction at COVID-19 is infection of supporting cells, that is, the virus acts on the neurons indirectly.