Viruses utilize cell surface glycans and plasma membrane receptors to attain an adequate attachment strength for initiating cellular entry. We show that SARS-CoV-2 particles bind to endogenous ACE2 receptors and added sialylated gangliosides in near-native membranes. This was explored using supported membrane bilayers (SMBs) that were formed using plasma membrane vesicles having endogenous ACE2 and GD1a gangliosides reconstituted in lipid vesicles. The virus binding rate to the SMBs is influenced by GD1a and inhibition of the ganglioside reduces the extent of virus binding to the membrane receptors. Using combinations of inhibition assays, we confirm that added GD1a in lipid membranes increases the availability of the endogenous ACE2 receptor and results in the synergistic binding of SARS-CoV-2 to the membrane receptors in SMBs.

中文翻译：

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SARS-CoV-2 与天然脂质膜中 ACE2 和神经节苷脂的协同结合

病毒利用细胞表面聚糖和质膜受体来获得足够的附着强度以启动细胞进入。我们发现 SARS-CoV-2 颗粒与内源 ACE2 受体结合，并在近天然膜中添加唾液酸化神经节苷脂。这是使用支持膜双层 (SMB) 进行探索的，该双层膜是使用具有在脂质囊泡中重构的内源 ACE2 和 GD1a 神经节苷脂的质膜囊泡形成的。病毒与 SMB 的结合率受 GD1a 的影响，抑制神经节苷脂会降低病毒与膜受体的结合程度。通过组合抑制测定，我们证实在脂质膜中添加 GD1a 会增加内源 ACE2 受体的可用性，并导致 SARS-CoV-2 与 SMB 中的膜受体协同结合。