Abstract
The omicron variant of severe acute respiratory syndrome coronavirus 2 causes much less olfactory dysfunction than the previous variants. There are several potential mechanisms for how omicron may change tissue tropism and spare olfactory function. The new mutations make omicron more hydrophobic and alkaline than previous variants, which may reduce penetration of the mucus layer. Overall, the new mutations minimally change receptor binding affinity, but entry efficiency into host cells is reduced in cells expressing transmembrane serine protease 2 (TMPRSS2). Because the support cells in the olfactory epithelium abundantly express TMPRSS2, these main target cells in the olfactory epithelium may become infected less by the new omicron variant.
Keywords: ACE2; COVID-19; D614G mutation; SARS-CoV-2; TMPRSS2; anosmia; loss of smell; mucus; omicron; prevalence.
【저자키워드】 COVID-19, SARS-CoV-2, ACE2, TMPRSS2, omicron, Anosmia, D614G mutation, Prevalence., Mucus, Loss of Smell, 【초록키워드】 coronavirus, Mutation, olfactory dysfunction, variants, Prevalence, D614G, Omicron variant, Receptor binding, Efficiency, Olfactory epithelium, host cell, tissue tropism, target cell, olfactory function, Support, acute respiratory syndrome, potential mechanism, transmembrane serine protease, hydrophobic, penetration, Express, Cell, reduced, less, cause, reduce, expressing, alkaline,