Non-neural expression of SARS-CoV-2 entry genes in the olfactory epithelium suggests mechanisms underlying anosmia in COVID-19 patients

David Brann; Tatsuya Tsukahara; Caleb Weinreb; Darren W. Logan; Sandeep Robert Datta

SARS-CoV-2 (CoV-2) is a pandemic coronavirus that causes the COVID-19 syndrome, which can include upper respiratory infection (URI) symptoms, severe respiratory distress, acute cardiac injury and death (1-4). CoV-2 is closely related to other beta-coronaviruses, including the causal agents in pandemic SARS and MERS (SARS-CoV and MERS-CoV, respectively) and endemic viruses typically associated with mild URI syndromes (hCoV-OC43 and hCoV-229E) (5) (6) (7) . Clinical reports suggest that infection with CoV-2 is associated with high rates of disturbances in smell and taste perception, including anosmia (8) (9) (10) (11) (12) (13) . These observations are consistent with a case report describing a SARS patient with long term anosmia (14) and with data demonstrating that olfactory function is commonly altered after infection with endemic coronaviruses (7, (15) (16) (17) (18) . While many viruses induce transient changes in odor perception due to inflammatory responses, in at least some cases COVID-related anosmia has been reported to occur in the absence of significant nasal inflammation or coryzal symptoms (12). This observation suggests that CoV-2 might directly target odor processing mechanisms, although the specific means through which CoV-2 alters odor perception remains unknown.