목적: Olfactory dysfunction has been identified in patients and several experimental animal models of COVID-19. Previous studies have shown that the non-neuronal cells are the primary targets for the SARS-CoV-2 in the olfactory epithelium. However, the mechanisms underlying olfactory dysfunction in patients with COVID-19 are still unclear. 방법:We intranasally inoculated 8-week-old K18-hACE2 transgenic mice with the 10²-10⁵ PFU of SARS-CoV-2 (strain hCoV19/Korea/KCDC9481/2020). Mice sacrificed at 2, 4, 7 and 10dpi were analyzed for changes in the upper and lower respiratory tracts, brain, and abdominal organs through histology and immunohistochemistry. In addition, the olfactory phenotype was investigated by performing avoidance tests. 결과:SARS-CoV-2 infection of K18-hACE2 mice caused a dose-dependent respiratory illness, contributing to death. Viral antigen was detected in the olfactory epithelium, particularly in the non-neuronal cell type, but not in the neuronal cells. We also found that the sequential recovery of the olfactory epithelium after 7dpi by confirming the reduction of expression level of target markers. In the avoidance test, mice infected with SARS-CoV-2 exhibited impaired olfactory function compared to uninfected mice. 결론:In summary, SARS-CoV-2-induced anosmia is caused by damage to non- neuronal cells rather than olfactory sensory neurons. These results suggest that inflammatory microenvironment rather than direct neuronal damage leads to olfactory dysfunction in COVID-19. Future studies would be required to investigate detailed mechanisms underlying olfactory dysfunction and subsequent recovery following SARS-CoV- 2 infection.