Inactivated SARS-CoV-2 Variant Omicron, Lineage B.1.1.529

The omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was initially discovered in South Africa and Botswana and reported to the World Health Organization (WHO) as a new variant on November 24, 2021. This new variant, also known as B.1.1.529, has spread rapidly and was designated a variant of concern (VOC) by the WHO on November 26, 2021. Further studies have shown that the omicron variant did not evolve from earlier known variants and exhibits some genomic differences. Three possible explanations for the formation of the omicron variant have been proposed: silent evolution in human populations with limited sequencing data; long-term evolution in a single or a small number of chronically infected individuals; or evolution in other animals, particularly rodents.

Currently, as many as 60 mutations have been identified in the BA.1 lineage, including 38 mutations in the spike (S) protein, one mutation in the envelope (E) protein, two mutations in the membrane (M) protein, and six mutations in the nucleocapsid (N) protein. The BA.2 lineage harbors 57 mutations, 31 of which are in the S protein. The S protein''s N-terminus differs significantly from that of BA.1. The S protein''s receptor-binding domain (RBD), responsible for binding to the host receptor angiotensin-converting enzyme 2 (ACE2), has the potential to enhance infectivity and mediate escape from vaccine-induced neutralizing antibodies. Therefore, mutations within the S protein''s RBD have garnered significant research attention. BA.1 and BA.2 share 12 mutations within the RBD, including G339D, S373P, S375F, K417N, N440K, S477N, T478K, E484A, Q493R, Q498R, N501Y, and Y505H. S371L, G446S, and G496S are found only in BA.1, while R346K is found in a member of the group, BA.1.1. BA.2 possesses two unique mutations in the RBD, including S371F and R408S, and shares T376A and D405N with BA.3. Some of these mutations have also been found in previous variants and are known to enhance viral infectivity, increase viral binding affinity, and promote antibody evasion.