Since the outbreak of COVID-19, many countries have reported cases of loss of smell due to infection with covid-19. Recently, a new study in the United States has revealed the mechanism, suggesting that loss of smell is likely to be a collateral consequence of inflammation after infection.
Olfactory dysfunction generally occurs early in the course of COVID-19 infection and is not directly related to disease severity and viral load. Previous studies have found that olfactory dysfunction is the earliest symptom in about 12% of patients with new coronary pneumonia. In most cases, symptoms resolve spontaneously within 3 to 4 weeks, but some patients develop persistent olfactory impairments for 12 months after infection.
In order to find out the olfactory pathological changes related to the new crown virus infection, the team participated in the Johns Hopkins University School of Medicine and the University of Maryland School of Medicine in the United States collected olfactory bulbs and olfactory tract tissue from the brains of 23 patients who died of new crown pneumonia, compared with the control group that was not infected with the new crown virus. The findings suggest that the loss of sense of smell is caused by infection of olfactory epithelial cells by the new crown virus, which in turn damages neurons, reduces the number of axons that can be used to send signals to the brain, and leads to dysfunction of the olfactory bulb.
Next, the researchers plan to conduct further follow-up studies in patients who died of infection with the Delta strains of the new coronavirus and the Omiljun strains to understand the extent to which different variants cause loss of smell.
(Editor: Yin Zi)