By analysing the oral cells of adult mice, scientists have found that a protein which the novel coronavirus uses to enter host tissue is not present in the taste buds, a finding which suggests that the loss of sense of smell reported by many COVID-19 patients might be due to inflammation triggered by the disease, and not directly caused by viral infection.
According to the study, published in the journal ACS Pharmacology & Translational Science, while the ACE2 receptor protein, used by the novel coronavirus SARS-CoV-2 to enter host tissue, was enriched in cells that give the tongue its rough surface, they couldn't be found in the cells of the taste buds.
The researchers, including those from the University of Georgia in the US, also showed that other viruses that affect taste, including the flu virus, might infect different tongue cell types.
They said viruses cause infection by invading specific cells in the body and reproducing, often damaging or killing those cells in the process.
While previous research had shown that SARS-CoV-2 enters human cells through the ACE2 receptor on the surface of some cells, including those of the human tongue, the current study found that this protein was not expressed specifically in taste bud cells by studying mice as a model organism.
Although the mouse version of ACE2 is not susceptible to SARS-CoV-2, the scientists said studying where it is expressed in mice could help clarify what happens when people become infected and lose the sense of taste.
When they analysed data from oral cells of mice at three developmental stages, the scientists found ACE2 in newborn mice but not in fetuses.
According to the researchers, previous studies in humans that were not focused on oral cells suggest ACE2 could be expressed at an early fetal stage and then again at a later stage.
They speculate that fetuses could have distinct susceptibilities to SARS-CoV-2 infection at different stages, adding that more work is needed to determine the timing and location of human ACE2 expression.