Design of potent membrane fusion inhibitors against SARS-CoV-2, an emerging coronavirus with high fusogenic activity

Yuanmei Zhu; Danwei Yu; Hongxia Yan; Huihui Chong; Yuxian He

The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.26.009233 doi: bioRxiv preprint peptide complexed with a HR2-derived peptide are higher than that of the SARS-CoV HR1 The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.26.009233 doi: bioRxiv preprint suggesting that it mainly utilizes a plasma membrane fusion pathway for cell entry. Sequence 232 analyses revealed that SARS-CoV-2 harbors the S1/S2 cleavage site in its S protein, although 233 its roles in S protein-mediated membrane fusion and viral life-cycle need to be characterized. 234 One can speculate that furin-mediated precleavage at the S1/S2 site in infected cells might The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.26.009233 doi: bioRxiv preprint infection assay as described previously (60). To produce pseudoviruses, HEK293T cells were 276 cotransfected with a backbone plasmid (pNL4-3.luc.RE) that encodes an Env-defective, The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.26.009233 doi: bioRxiv preprint The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.26.009233 doi: bioRxiv preprint 23 545 author/funder. All rights reserved. No reuse allowed without permission.