SARS-CoV-2 infects and damages the mature and immature olfactory sensory neurons of hamsters.

摘要: Background Coronavirus Disease 2019 (COVID-19) is primarily an acute respiratory tract infection. Distinctively, a substantial proportion of COVID-19 patients develop olfactory dysfunction uncertain underlying mechanism which can be severe and prolonged. The roles inflammatory obstruction the clefts leading to conductive impairment, cytokines affecting neuronal function, destruction neurons or their supporting cells, direct invasion bulbs, in causing are uncertain. Methods In this study, we investigated location for pathogenesis SARS-CoV-2 from epithelium (OE) nasopharynx bulb golden Syrian hamsters. Results After intranasal inoculation with SARS-CoV-2, cell infiltration proinflammatory cytokine/chemokine responses were detected nasal turbinate tissues peaked between 2 4 days post-infection highest viral load at day post-infection. Besides nasopharyngeal pseudo-columnar ciliated epithelial antigens also more superficial mature sensory labeled by marker protein (OMP), less labelled Tuj1 basal position, sustentacular cells provide metabolic physical support neurons, resulting apoptosis OE. During whole course infection, not bulb. Conclusions inflammation OE, infection immature may contribute unique reported SARS-CoV.