Table 2.

Molecular mechanisms of immune evasion by the SARS-CoV-2 variants

Lineage	Mutations	Functions	Mechanisms	Ref
B.1.1.7	N501Y E484K	Mutation 501 Y enhances the affinity of RBD to ACE2; A π-π interaction enhances RBD binding to ACE2 and eliminates potent neutralizing antibody binding.	Perform immune escape by disrupting antibody binding; the upregulating of Orf6 and Orf9b has contributed to the increased ability of immune evasion.	(Starr et al., 2020; Supasa et al., 2021; Yang et al., 2021; Thorne et al., 2022)
B.1.351	K417N E484K N501Y	N501Y and E484K have increased binding of RBD and ACE2.	N501Y and E484K have increased binding of RBD and ACE2.	(Zhou et al., 2021)
B.1.1.28	N501Y E484K	Resistance to neutralization by nAb, including naturally acquired and vaccination-induced resistance.	E484K and N501Y increase the binding affinity of S protein to ACE2.	(Gobeil et al., 2021; Tegally et al., 2020)
B.1.617.2	L452R	S2X303 can cross-react with multiple mutant strains compared with other neutralizing antibodies.	The L452R has a stronger affinity for ACE2 receptor and reduces the recognition ability of the immune system.	(McCallum et al., 2021c; Zhang et al., 2021)
B.1.1.529	K417N, G446S, E484A, Q493R	Mutations can cause immune evasion of the novel coronavirus. Omicron strains have enhanced spread owing to enhanced S protein consistency.	Omicron Spike Trimer has enhanced stability. K417N, G446S, E484A, and Q493R bypass neutralizing antibodies whose epitopes overlap with the ACE2-binding motif.	(Fang and Shi, 2022; Johnson et al., 2021; Shuai et al., 2022; Cui et al., 2022)