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

The identification of non-neuronal cell types in the OE and bulb susceptible to CoV-2 infection suggests three possible, non-mutually-exclusive mechanisms for the acute loss of smell reported in COVID-19 patients. First, local infection of support cells and vascular pericytes in the nose and bulb could cause significant inflammatory responses whose downstream effects could alter the function of OSNs or bulb neurons. Second, damage to support cells (which are responsible for local water balance and ionic balance) could indirectly influence signaling from OSNs to the brain; our finding that a subset of microvillar cells are homologues of pulmonary ionocyteswhich play a key role in maintaining extracellular chloride gradients in the lungis consistent with this model (48). Finally, damage to sustentacular cells and Bowman's gland cells in mouse models leads to diffuse architectural damage to the entire OE, which could abrogate smell perception (49) .