Introduction: B.1.526-E484K and B.1.526-S477N share the characteristic spike protein mutations L5F, T95I, D253G, D614G and either A701V or Q957R, along with either E484K or S477N.
Introduction: Isolates subsequently branched into four sub-lineages, with two major groups B.1.526-E484K and B.1.526-S477N containing A701V, and a smaller sub-lineage B.1.526-S477N containing Q957R.
Introduction: Pseudoviruses were constructed conta
GB-2 blocking the interaction between ACE2 and wild type and mutation of spike protein of SARS-CoV-2.
Introduction: The SARS-CoV-2 beta variant contains nine mutations in the spike protein: D614G, Delta242-Delta244, and R246I in the N-terminal domain; three mutations (K417N, E484K, and N501Y) in the RBD; and one mutation (A701V) near the furin cleavage site.
Detection and characterization of the SARS-CoV-2 lineage B.1.526 in New York.
Abstract: The most common sets of spike mutations in this lineage (now designated as B.1.526) are L5F, T95I, D253G, E484K or S477N, D614G, and A701V.
Method: Human plasma samples were assayed for neutralization activity against lentiviruses pseudotyped with SARS-CoV-2 spike containing a 21-amino acid cytoplasmic tail deletion and either D614G or mutations corresponding to lineage B.1.526 (v.1: L5F, T95I, D253G, E484K, D614G, and A701V; v.
Phylogenomic analysis of SARS-CoV-2 from third wave clusters in Malaysia reveals dominant local lineage B.1.524 and persistent spike mutation A701V.
Abstract: This lineage contains another spike mutation A701V that co-exists with the D614G spike mutation that was predominant in most of the third-wave clusters.
Modelling conformational state dynamics and its role on infection for SARS-CoV-2 Spike protein variants.
SARS_CoV_2 mutation literature information.
PMID: 
2021
Signal transduction and targeted therapy
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