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Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV.
Nature Communications ( IF 14.7 ) Pub Date : 2020-03-27 , DOI: 10.1038/s41467-020-15562-9
Xiuyuan Ou 1 , Yan Liu 1 , Xiaobo Lei 1 , Pei Li 1 , Dan Mi 1 , Lili Ren 1 , Li Guo 1 , Ruixuan Guo 1 , Ting Chen 1 , Jiaxin Hu 1 , Zichun Xiang 1 , Zhixia Mu 1 , Xing Chen 2 , Jieyong Chen 3 , Keping Hu 2 , Qi Jin 1 , Jianwei Wang 1 , Zhaohui Qian 1
Affiliation  

Since 2002, beta coronaviruses (CoV) have caused three zoonotic outbreaks, SARS-CoV in 2002-2003, MERS-CoV in 2012, and the newly emerged SARS-CoV-2 in late 2019. However, little is currently known about the biology of SARS-CoV-2. Here, using SARS-CoV-2 S protein pseudovirus system, we confirm that human angiotensin converting enzyme 2 (hACE2) is the receptor for SARS-CoV-2, find that SARS-CoV-2 enters 293/hACE2 cells mainly through endocytosis, that PIKfyve, TPC2, and cathepsin L are critical for entry, and that SARS-CoV-2 S protein is less stable than SARS-CoV S. Polyclonal anti-SARS S1 antibodies T62 inhibit entry of SARS-CoV S but not SARS-CoV-2 S pseudovirions. Further studies using recovered SARS and COVID-19 patients' sera show limited cross-neutralization, suggesting that recovery from one infection might not protect against the other. Our results present potential targets for development of drugs and vaccines for SARS-CoV-2.

中文翻译:

SARS-CoV-2刺突糖蛋白对病毒侵入的表征及其与SARS-CoV的免疫交叉反应。

自 2002 年以来,β 冠状病毒 (CoV) 已引起 3 次人畜共患病暴发:2002-2003 年的 SARS-CoV、2012 年的 MERS-CoV 和 2019 年底新出现的 SARS-CoV-2。然而,目前对其生物学知之甚少SARS-CoV-2。在这里,我们使用 SARS-CoV-2 S 蛋白假病毒系统,确认人血管紧张素转化酶 2(hACE2)是 SARS-CoV-2 的受体,发现 SARS-CoV-2 主要通过内吞作用进入 293/hACE2 细胞, PIKfyve、TPC2 和组织蛋白酶 L 是进入的关键,SARS-CoV-2 S 蛋白的稳定性不如 SARS-CoV S。多克隆抗 SARS S1 抗体 T62 抑制 SARS-CoV S 的进入,但不抑制 SARS-CoV -2 S 假病毒。使用恢复的 SARS 和 COVID-19 患者血清的进一步研究显示交叉中和作用有限,这表明从一种感染中恢复可能无法预防另一种感染。
更新日期:2020-04-24
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