Olfactory Epithelium Infection by SARS-CoV-2: Possible Neuroinflammatory Consequences of COVID-19

The loss of smell is a typical diagnostic symptom of coronavirus disease 2019 (COVID-19). This sensorial deprivation may be expressed as quantitative (anosmia or hyposmia) or qualitative (dysosmia) alterations as a consequence of anatomical disturbances of the nasal epithelium structure. The olfactory system sends direct neuronal connections to brain structures that are involved in emotional processing, including deep temporal nuclei. This anatomical and functional feature may be related to the occurrence of emotional disorders among COVID-19 patients.

We identify a possible sequence of events, from typical olfactory dysfunction that is associated with COVID-19 and caused by olfactory epithelium damage to disturbances in the quality of life and emotional state of infected patients that is attributable to possible neuroinflammatory processes. Sensorial deprivation causes deleterious actions on mood, negatively affecting quality of life. Olfactory dysfunction that is associated with COVID-19 occurs concurrently with psychological distress, symptoms of anxiety, and depressive disorders and impinges on self-perceived quality of life.

Changes in mood are certainly associated with multiple factors, including the environment and isolation, but the observation that the virus may penetrate the central nervous system through the olfactory bulb and the connection between the olfactory system and prefrontal and orbitofrontal cortices and the amygdala-hippocampus do not allow one to discard neural factors that are involved in the pathophysiology of emotional symptoms in post-COVID-19 patients. Behavioral symptoms of COVID-19 involve local olfactory actions and the participation of central neuronal systems.