Abstract
A SARS-like coronavirus 2 (SARS-CoV-2) has caused a pandemic Coronavirus Disease 2019 (COVID-19) that killed more than 3.3 million people worldwide. Like the SARS-CoV, SARS-CoV-2 also employs a receptor-binding motif (RBM) of its spike protein to bind a host receptor, the angiotensin-converting enzyme 2 (ACE2), to gain entry. Currently, several mRNA or adenoviral vaccines encoding for the spike protein of SARS-CoV-2 are being used to boost antibodies capable of inhibiting spike-ACE2 interaction and viral entry. However, recent evidence has also suggested an anti-inflammatory effect of spike-reactive antibodies, suggesting that some SARS-CoV-2 spike-based vaccines may elicit protective antibodies capable of inhibiting GM-CSF production and COVID-19 progression.
Highlights
The recent emergence and rapid spread of SARS-like coronavirus 2, SARS-CoV-2, has caused a pandemic COVID-19 that is catastrophically harming human health (Qiang et al 2021)
Neutralizing antibodies targeting the receptor-binding domain (RBD) or the receptor-binding motif (RBM) of SARS-CoV-2 S protein were found in the blood of COVID-19 patients (Zost et al 2020; Pinto et al 2020), and some of which could impair viral entry (Zost et al 2020; Pinto et al 2020)
Li et al Mol Med (2021) 27:49 we have recently generated recombinant protein corresponding to the receptor binding domain (RBD, residue 319–541) and receptor binding motif (RBM, residue 437– 508) of SARS-CoV-2 spike (S) protein, and employed them to assess the angiotensin-converting enzyme 2 (ACE2)-binding properties and screen for RBM-binding Monoclonal antibodies (mAb) using Surface Plasma Resonance (SPR) technique (Qiang et al 2021)
Summary
The recent emergence and rapid spread of SARS-like coronavirus 2, SARS-CoV-2, has caused a pandemic COVID-19 that is catastrophically harming human health (Qiang et al 2021). Neutralizing antibodies targeting the receptor-binding domain (RBD) or the receptor-binding motif (RBM) of SARS-CoV-2 S protein were found in the blood of COVID-19 patients (Zost et al 2020; Pinto et al 2020), and some of which could impair viral entry (Zost et al 2020; Pinto et al 2020).
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