To investigate the histopathological alterations in the olfactory system of COVID-19 patients and elucidate the underlying mechanisms contributing to anosmia. 

Since its discovery, SARS-CoV-2 has caused a global pandemic claiming millions of lives. The onset of such a widespread infection brought numerous diagnostic variabilities and chronic pathologies, one being the complete loss of smell or anosmia. Investigating our hypothesis led to understanding the infection pathways and mechanisms underlying these chemosensory deficits.

We compared and analyzed the olfactory epithelia of healthy and infected individuals showing the extent of damage and the impairment that arises from the nasal instillation of the SARS-CoV-2 virus. Furthermore, we examined the functional contribution of the underlying histopathology of the cortical tissue comprising the olfactory bulb in causing damage to olfactory function. We also conducted a study on the role of the immune response as well as persistent viral exposure in causing dysfunction in the processing of olfactory stimuli in the brain.

The results showed the presence of histological changes in the frontal lobe of the brain as well as necrotizing olfactory bulbitis of the olfactory bulb. The viral entry and infection resulted in prominent changes in the olfactory epithelium including the death of sustentacular cells along with intracranial manifestation. Diffuse infiltrating immune cell response caused disorganization of the olfactory sensory neurons hindering the olfactory stimuli processing.

Through our findings, it was evident that olfactory dysfunction arises from the interaction between peripheral olfactory receptor damage due to local inflammation and viral invasion, along with central nervous system involvement. Our research aimed to use histopathological studies to summarize the onset and causes of anosmia in COVID-19 patients and to further investigate multiple system interactions as a possible mechanism of SARS-CoV-2–induced olfactory dysfunction.