Selected article for: "host cell and SARS share"
Author: Xin Zeng; Lingfang Li; Jing Lin; Xinlei Li; Bin Liu; Yang Kong; Shunze Zeng; Jianhua Du; Huahong Xiao; Tao Zhang; Shelin Zhang; Jianghai Liu
Title: Blocking antibodies against SARS-CoV-2 RBD isolated from a phage display antibody library using a competitive biopanning strategy
  • Document date: 2020_4_20
    • ID: 4w6caxwu_2
    Snippet: The primary sequences of S protein between severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 share about 76% identities and 86% similarities, which indicates high possibility of structural homology and the same infection pathway. SARS-CoV and SARS-CoV-2 recognized the same host cell receptor ACE2 for mediating viral entry into host cells. It was reported that SARS-CoV S protein trimer bound to ACE2 at 1:1 in ratio [1, 2] . B.....
    Document: The primary sequences of S protein between severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 share about 76% identities and 86% similarities, which indicates high possibility of structural homology and the same infection pathway. SARS-CoV and SARS-CoV-2 recognized the same host cell receptor ACE2 for mediating viral entry into host cells. It was reported that SARS-CoV S protein trimer bound to ACE2 at 1:1 in ratio [1, 2] . Before infection, RBD of each SARS-CoV S monomer was partially buried in the inactive "down" conformation and not able to bind ACE2 due to steric clash. Once infection started, one monomer turned "up" its RBD to expose enough space to ACE2, inducing further conformational open and loose for proteolysis [1, 3] . Atomic-level structural analysis suggested that the spatial interaction and interface between SARS-CoV-2 RBD and ACE2 was mostly in accordance with the SARS-CoV case [4] . Besides, a Cryo-EM structure of SARS-CoV-2 S protein trimer published recently showed that one of the three RBDs was in "up" conformation and naturally exposed the whole interaction interface [5] , while the classic closed symmetric trimer still existed [6] . That might explain why SARS-CoV-2 is much more contagious than SARS-CoV and causing tricky problems worldwide.

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