PDF(Pubmed)
Abstract：
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections can cause loss or alteration of taste and smell as early symptoms or sequelae, but the detailed mechanism behind this phenomenon remains unclear. Here, we investigated whether the SARS-CoV-2 spike protein induces taste cell apoptosis and expression of the apoptosis-related cytokine TNF-α in male Sprague-Dawley rats. Terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-fluorescein nick end labeling (TUNEL) assay results revealed a significantly higher apoptosis index for taste cells in the SARS-CoV-2 group than for those in the control group. An immunohistochemistry analysis indicated significantly more TNF-α-positive cells in the SARS-CoV-2 group compared with the control group. These data suggest that the SARS-CoV-2 spike protein promotes taste cell apoptosis and the release of apoptosis-related cytokine TNF-α, implicating its contribution to the taste malfunction caused by coronavirus disease 2019 (COVID-19).
摘要：
严重急性呼吸道综合症冠状病毒2（SARS-CoV-2）感染可导致味觉和嗅觉丧失或改变，作为早期症状或后遗症，但这种现象背后的详细机制仍不清楚。这里,我们研究了SARS-CoV-2刺突蛋白是否诱导雄性Sprague-Dawley大鼠味觉细胞凋亡和凋亡相关细胞因子TNF-α的表达。末端脱氧核苷酸转移酶（TdT）介导的脱氧尿苷三磷酸（dUTP）-荧光素缺口末端标记（TUNEL）测定结果表明，SARS-CoV-2组的味觉细胞凋亡指数明显高于对照组。免疫组化分析表明，SARS-CoV-2组的TNF-α阳性细胞明显多于对照组。这些数据表明SARS-CoV-2刺突蛋白促进味觉细胞凋亡和释放凋亡相关细胞因子TNF-α，暗示其对2019年冠状病毒病(COVID-19)引起的味觉障碍的贡献。
