SARS-CoV-2 variants, spike mutations and immune escape. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Mechanisms of SARS-CoV-2 entry into cells. Structural insights into coronavirus entry. Host cell entry of Middle East respiratory syndrome coronavirus after two-step, furin-mediated activation of the spike protein. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. The coronavirus spike protein is a class I virus fusion protein: structural and functional characterization of the fusion core complex. Viral targets for vaccines against COVID-19. Omicron spike function and neutralizing activity elicited by a comprehensive panel of vaccines. COVID-19 vaccine effectiveness against the omicron (BA.2) variant in England. Occurrence and significance of Omicron BA.1 infection followed by BA.2 reinfection. Protection of Omicron sub-lineage infection against reinfection with another Omicron sub-lineage. Cross-neutralization of Omicron BA.1 against BA.2 and BA.3 SARS-CoV-2. Omicron BA.2 specifically evades broad sarbecovirus neutralizing antibodies. Antigenic cartography of SARS-CoV-2 reveals that Omicron BA.1 and BA.2 are antigenically distinct. Neutralization of the SARS-CoV-2 Omicron BA.1 and BA.2 variants. SARS-CoV-2 Omicron sublineages exhibit distinct antibody escape patterns.
Antibody evasion properties of SARS-CoV-2 Omicron sublineages.
Clinical severity of omicron lineage BA.2 infection compared with BA.1 infection in South Africa. Virological characteristics of the SARS-CoV-2 Omicron BA.2 spike. COVID-19 mortality and vaccine coverage - Hong Kong Special Administrative Region, China, January 6, 2022–March 21, 2022. Epidemiology of infections with SARS-CoV-2 Omicron BA.2 variant, Hong Kong, January–March 2022. Household transmission of SARS-CoV-2 Omicron variant of concern subvariants BA.1 and BA.2 in Denmark. SARS-CoV-2 Omicron sublineage BA.2 replaces BA.1.1: genomic surveillance in Japan from September 2021 to March 2022. These results suggest that both immune evasion and replicative advantage may contribute to the heightened transmissibility of the Omicron subvariants. As in BA.1, mutations in the BA.2 S remodel its antigenic surfaces, leading to strong resistance to neutralizing antibodies. Both BA.1 and BA.2 viruses replicated substantially faster in animal lungs than the early G614 (B.1) strain in the absence of pre-existing immunity, possibly explaining the increased transmissibility despite their functionally compromised spikes. BA.2 S can fuse membranes slightly more efficiently than Omicron BA.1, but still less efficiently than other previous variants.
Here, we have characterized structural, functional and antigenic properties of the full-length BA.2 spike (S) protein and compared replication of the authentic virus in cell culture and an animal model with previously prevalent variants.
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