If you have been wondering why many Covid-19 infected people reported loss of smell, then US researchers probably have discovered the answer. They found that infection with the SARS-CoV-2 indirectly dials down the action of olfactory receptors, proteins on the surfaces of nerve cells in the nose that detect the molecules associated with odors.
Published online in the journal Cell, the study led by researchers from NYU Grossman School of Medicine and Columbia University, also shed light on the effects of COVID-19 on other types of brain cells and other lingering neurological effects of COVID-19 such as “brain fog,” headaches, and depression.
Experiments showed that the presence of the virus near nerve cells (neurons) in olfactory tissue brought an inrushing of immune cells, microglia, and T cells that sense and counter infection. Such cells release proteins called cytokines that change the genetic activity of olfactory nerve cells, even though the virus cannot infect them, say the study authors. Where immune cell activity would dissipate quickly in other scenarios, in the brain, according to the team’s theory, immune signaling persists in a way that reduces the activity of genes needed for the building of olfactory receptors.
“Our findings provide the first mechanistic explanation of smell loss in COVID-19 and how this may underlie long COVID-19 biology,” said co-corresponding author Benjamin tenOever, professor in the Departments of Medicine and Microbiology at NYU Langone Health.
“The work, in addition to another study from the tenOever group, also suggests how the pandemic virus, which infects less than 1 percent of cells in the human body, can cause such severe damage in so many organs.”