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Wanwisa Dejnirattisai et al.
Summary: On November 24, 2021, the sequence of a new SARS-CoV-2 variant, Omicron-B.1.1.529, was announced. Compared to previous variants, Omicron has a higher number of mutations in the Spike (S) protein. Serum neutralization of Omicron by individuals vaccinated or previously infected with Alpha, Beta, Gamma, or Delta variants is significantly reduced or ineffective. Third vaccine doses can boost neutralization titers against Omicron, and high titers are observed in both vaccinated individuals and those infected with the Delta variant. Most potent monoclonal antibodies and antibodies under development are unable to effectively neutralize Omicron due to mutations in its Spike protein. Omicron has structural changes compared to earlier viruses and utilizes mutations that enhance its binding to ACE2, allowing for immune escape. This results in a large number of mutations in the ACE2 binding site and a rebalancing of receptor affinity similar to earlier pandemic viruses.
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Summary: The COVID-19 pandemic has caused a global outbreak, with hopes pinned on effective vaccines and antibody treatments. However, the virus continues to mutate, with the E484K mutation potentially increasing transmissibility and reducing antibody effectiveness. Research shows that the E484K mutation enhances virus-receptor binding affinity while diminishing antibody binding strength.
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Daming Zhou et al.
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Constantinos Kurt Wibmer et al.
Summary: The SARS-CoV-2 virus in the B.1.351 variant discovered in South Africa can evade neutralization by most antibodies when expressed, but does not affect binding by convalescent plasma. This suggests the potential for reinfection with antigenically distinct variants and predicts reduced efficacy of spike-based vaccines.
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Kai Wu et al.
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Victoria Jane Hall et al.
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Ge Song et al.
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Teresa Aydillo et al.
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Hannah Chung et al.
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BMJ-BRITISH MEDICAL JOURNAL
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Benjamin Israelow et al.
Summary: Research demonstrates that both humoral and cellular immunity play a role in clearing SARS-CoV-2, and convalescent mice or mice vaccinated with mRNA are protected from infection with both the wild type virus and the B.1.351 variant. This protection is mainly mediated by antibody response rather than cellular immunity.
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