Temporary loss of smell or anosmia is the key common neurological symptom found in Covid-19 patients. The underlying mechanisms behind anosmia in Covid-19 patients have been vague.
According to a new study led by neuroscientists at Harvard Medical School, coronavirus infection affects olfactory support cells, not neurons. The new research which is published in the journal Science Advances found that the olfactory cell types are most vulnerable to infection by SARS-CoV-2 (the virus responsible for causing Covid-19). But unexpectedly, the sensory neurons that are responsible for detecting and transmitting the sense of smell to the brain are not among the cell types which are vulnerable to COVID virus.
Senior study author Sandeep Robert Datta, Associate Professor in the Blavatnik Institute at Harvard Medical School said, “Our findings indicate that the novel coronavirus changes the sense of smell in patients not by directly infecting neurons but by affecting the function of supporting cells”.
He added, “This implies that in most cases, SARS-CoV-2 infection is unlikely to permanently damage olfactory neural circuits and lead to persistent anosmia (a condition related to a variety of mental and social health issues such as depression and anxiety). 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. But we need more data and a better understanding of the underlying mechanisms to confirm this conclusion.”
In the study, Datta and colleagues worked on finding how the sense of smell gets changed in Covid-19 patients through the identification of cell types most vulnerable to SARS-CoV-2 infection. They analysed the existing single-cell sequencing datasets that contained the information of genes expressed by hundreds of thousands of individual cells in the upper nasal cavities of humans, mice and nonhuman primates.
The research found that olfactory sensory neurons do not express the gene that encodes the ACE2 receptor protein that is used by SARS-CoV-2 to enter the human cells. Instead, ACE2 is expressed in cells which give the metabolic and structural support to olfactory sensory neurons and also to certain populations of stem cells and blood vessel cells.
The study concluded that infection of non-neuronal cell types may be responsible for anosmia in Covid-19 patients. The finding will help in understanding the progression of the disease in a better way.