The study investigates the expression of SARS-CoV-2 entry genes in the olfactory system to understand the mechanisms underlying COVID-19-associated anosmia. Using bulk and single-cell RNA sequencing, the researchers found that support and stem cells in the human and mouse olfactory epithelium, as well as vascular pericytes in the mouse olfactory bulb, express angiotensin-converting enzyme 2 (ACE2), which is essential for SARS-CoV-2 cell entry. In contrast, ACE2 was not detected in olfactory sensory neurons or olfactory bulb neurons. Immunostaining confirmed these results, showing pervasive expression of ACE2 in sustentacular cells and pericytes. These findings suggest that infection of non-neuronal cell types leads to olfactory dysfunction in patients with COVID-19. The study also explores the distribution of ACE2 and TMPRSS2 in the mouse olfactory bulb, finding that these genes are expressed in vascular pericytes but not in neurons. The authors propose that primary infection of non-neuronal cell types may be responsible for anosmia in COVID-19 patients, and discuss potential mechanisms, including inflammatory responses and damage to support cells.The study investigates the expression of SARS-CoV-2 entry genes in the olfactory system to understand the mechanisms underlying COVID-19-associated anosmia. Using bulk and single-cell RNA sequencing, the researchers found that support and stem cells in the human and mouse olfactory epithelium, as well as vascular pericytes in the mouse olfactory bulb, express angiotensin-converting enzyme 2 (ACE2), which is essential for SARS-CoV-2 cell entry. In contrast, ACE2 was not detected in olfactory sensory neurons or olfactory bulb neurons. Immunostaining confirmed these results, showing pervasive expression of ACE2 in sustentacular cells and pericytes. These findings suggest that infection of non-neuronal cell types leads to olfactory dysfunction in patients with COVID-19. The study also explores the distribution of ACE2 and TMPRSS2 in the mouse olfactory bulb, finding that these genes are expressed in vascular pericytes but not in neurons. The authors propose that primary infection of non-neuronal cell types may be responsible for anosmia in COVID-19 patients, and discuss potential mechanisms, including inflammatory responses and damage to support cells.