Temporary loss of smell, known as anosmia, is one of the most common early indicators of COVID-19. Although some say it may even be more accurate in predicting infection by the virus than having a fever or cough, the underlying mechanisms behind it have been unknown until now.
Although olfactory cells do not have the ACE2 receptor protein (the protein COVD-19 most commonly uses to infect cells and replicate from), the protein is expressed in cells that structurally support olfactory sensory neurons, as well as some stem and blood vessel cells. Thus, the researchers suggest that infection of nonneuronal cell types may lead to a loss of smell in patients with COVID-19.
The findings also imply that infection by SARS-CoV-2 is unlikely to leave permanent damage on olfactory neural circuits nor lead to permanent or long term loss of smell.
“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,” says senior author of the study, Sandeep Robert Datta. “But we need more data and a better understanding of the underlying mechanisms to confirm this conclusion.”
So far, data analyses show that most COVID-19 patients are likey to have some level of anosmia, although it is usually temporary. Analyses of electronic health records indicate that people with COVID-19 are 27 times more likely to have a loss in smell, whereas only around 2.2 to 2.6 times as likely to have a fever, cough, or other respiratory problem, than those without the virus.
The researchers hope their findings will accelerate efforts to better understand how anosmia works in patients with COVID-19. They hope that this understanding may then evolve into better treatments for the condition and the development of better smell-based diagnostics for those infected with the virus.
Sources: Neuroscience News, Technology Networks
