Figure 1.

The biological characteristics of key amino acid mutations of Spike in B.1.1.7 and B.1.617.2 variant. Mutations (HV69‐70del, N501Y, D614G, P681H/R, L452R, T478K) could increase the binding affinity and binding tightness of SARS‐CoV‐2 spike to hACE2 receptor, or increase cell‐cell membrane fusion, result in increasing the infectivity of B.1.1.7 and B.1.617.2 variant. 144del and L452R mutations generated resistance to the neutralization activity of mAbs, convalescent plasma, and post‐vaccination serum against B.1.1.7 and B.1.617.2 variant, respectively. del, deletion; FP, fusion peptide; HR1, heptad repeat 1; HR2, heptad repeat 2; IC, intracellular domain; NTD, N‐terminal domain; RBD, receptor‐binding domain; RBM, receptor binding motif; SD1, subdomain 1; SD2, subdomain 2; TD, transmembrane domain