Plausible cellular basis for loss of smell in COVID-19 patients, finds AIIMS-IIIT study

New Delhi: A research on the reason for the loss of smell in COVID-19 patients, conducted by All India Institute of Medical Sciences (AIIMS) and IIIT has found a plausible cellular basis for the loss of smell in patients infected with the novel Coronavirus.

"This is the first-ever research that came out to find the reason behind the loss of smell in COVID cases," one of the researchers, Dr Jatin Ahuja, DM Infectious Diseases at AIIMS told Millennium Post.

A prominent clinical symptom of the 2019-novel coronavirus (nCoV) infection is hyposmia or anosmia (decrease or loss of sense of smell), along with general symptoms such as fatigue, shortness of breath, fever and cough.

"The identity of the cell lineages that underpin the infection-associated loss of olfaction could be critical for the clinical management of 2019-nCoV-infected individuals. Recent research has confirmed the role of angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) as key host-specific cellular moieties responsible for the cellular entry of the virus," the study said.

The report has also examined the autopsy of those who have died of the infection and revealed that the organs or tissues with high expression levels of certain cells and viral-entry associated genes are most vulnerable to the infection.

"Accordingly, the ongoing medical examinations and the autopsy reports of the deceased individuals indicate that organs/tissues with high expression levels of ACE2, TMPRSS2 and other putative viral entry-associated genes are most vulnerable to the infection. We studied if anosmia in 2019-nCoV-infected individuals can be explained by the expression patterns associated with these host-specific moieties across the known olfactory epithelial cell types, identified from a recently published single-cell expression study. Our findings underscore selective expression of these viral entry-associated genes in a subset of sustentacular cells (SUSs), Bowman's gland cells (BGCs) and stem cells of the olfactory epithelium. Co-expression analysis of ACE2 and TMPRSS2 and protein-protein interaction among the host and viral proteins elected regulatory cytoskeleton protein-enriched SUSs as the most vulnerable cell type of the olfactory epithelium," the research paper stated.

Furthermore, the expression, structural and docking analyses of cell ACE2 revealed the potential risk of olfactory dysfunction in four additional mammalian species, revealing evolutionarily conserved infection susceptibility. "In summary, our findings provide a plausible cellular basis for the loss of smell in 2019-nCoV-infected patients," the paper added.