Abstract: We report high frequency mutations with improved binding affinity to ACE2 including S477N, N439K, V367F, and N501Y and address the potential impact of RBD mutations on antibody binding.
Conclusion: In conclusion, we found a number of high frequency SARS-CoV-2 RBD mutations with improved binding affinities to the ACE2 receptor including S477N, N4
Introduction: We found four high frequency variants with improved binding to ACE2:S477N, N439K, V367F, and N501Y and cross-referenced antibody interaction data with RBD mutations.
GB-2 blocking the interaction between ACE2 and wild type and mutation of spike protein of SARS-CoV-2.
Discussion: Because these N501Y, K417N, E484K and L452R mutations in RBD play the important role in immune evasion, we focused on the effect of GB-2 on these mutations.
Discussion: Both alpha and beta variants have the N501Y mutation.
Discussion: GB-2 can inhibit the binding between ACE2 and RBD with the triple mutation (K417N-E484K-N501Y).
Discussion: However, the combination of the E484K, K417N, and N501Y mutations could induce a higher degree of conformational alterations of the RBD
EGCG as an anti-SARS-CoV-2 agent: Preventive versus therapeutic potential against original and mutant virus.
2Conclusion: In vitro and in silico data indicate that EGCG binds the N501Y
Abstract: Molecular modeling experiments revealed N501Y-specific stacking interactions in the RBD-ACE2 complex and provided insight into EGCG interference with the complex formation.
Abstract: We complemented that finding with a detailed investigation of EGCG interactions with viral S-protein subunits, including S2, RBD, and the RBD mutant harboring the N501Y mutation.
Result: We considered two variants of the receptor binding domain: the consensus one (RBD) and its analog harboring the N501Y mutation in the ACE2-binding site (RBDm).
Introduction: N501Y enhances receptor binding domain/angiotensin-converting enzyme 2 (ACE2) receptor binding affinity while also disrupting the binding of potent neutralizing antibodies and is the major S determinant driving increased transmission of these variants.
Introduction: Gamma variant has three changes in the S RBD (K417T, E484K, and N501Y).
Introduction: The B.1.1.7 variant, now labelled Alpha variant, carries the N501Y mutation in the S receptor-binding domain (RBD) whereas the B.1.351 variant, labelled Beta variant, has three notable mutations in the S
SARS-CoV-2 variant prediction and antiviral drug design are enabled by RBD in vitro evolution.
Abstract: Further in vitro evolution increased binding by 1,000-fold and identified mutations that may be more infectious if they evolve in the circulating viral population, for example, Q498R is epistatic to N501Y.
Abstract: We found that mutations present in more transmissible viruses (S477N, E484K and N501Y) were preferentially selected in our high-throughput screen.
A Genomic Snapshot of the SARS-CoV-2 Pandemic in the Balearic Islands.
Discussion: This lineage is defined by 14 amino acid changes and three deletions, including six amino acid substitutions and two deletions in the spike protein: S:DeltaH69-V70, S:DeltaY144, S:N501Y, S:A570D, S:P681H, S:T716I, S:S982A, and S:D1118H and it has been related with some evolutionary advantages such as an increased transmissibility.
Molecular Characterization of Severe Acute Respiratory Syndrome Coronavirus 2 Isolates From Central Inner Sardinia.
Result: The III wave was characterized by the appearance of the subset of mutations that distinguish the B.1.1.7 lineage such as H69_V70del, Y144del, N501Y
Discussion: Spike N501Y was associated with a slight but significant reduction in neutralization.
Discussion: All these substitutions were associated with the B.1.1.7 lineage, besides spike N501Y which also characterizes P.1 and B.1.351 lineages, as their corresponding clade nomenclature suggests.
Discussion: Other substitutions were found in specific lineages, such as spike H69_V70del, Y144del, N501Y, or nucleocapsid S235F.
Antidepressant and Antipsychotic Drugs Reduce Viral Infection by SARS-CoV-2 and Fluoxetine Shows Antiviral Activity Against the Novel Variants in vitro.
Introduction: A common RBD mutation, N501Y, is shared by alpha, beta, and gamma, while K417N and E484K are found in beta and gamma.
Introduction: Moreover, infection by pseudotyped viruses carrying N501Y, K417N, or E484K single point mutations or triple mutation (N501Y/K417N/E484K) in the spike protein was shown to be reduced by fluoxetine.
Result: We found that fluoxetine (10 microM) treatment for 24 h was effective against pseudotyped viruses carrying single point mutations in their S protein (N501Y, PMID: 35140714
2021
Frontiers in immunology
Result: By contrast, N501Y slightly strengthens the binding, establishing a hydrogen bond with D57 in CDRH2 ( Figure 4B ).
Importation, circulation, and emergence of variants of SARS-CoV-2 in the South Indian state of Karnataka.
Introduction: Viruses of the lineage B.1 have acquired several other amino acid replacements in the Receptor Binding Domain of the Spike protein - specifically in the lineages which have been designated as VOCs, namely -B.1.1.7 (N501Y), B.1.351 (N501Y, E484K, K417T) and P.1 from the line
Result: The N501Y change was confined to the B.1.1.7 lineage.
Discussion: All nine amino acid changes, namely N440K, S477N, V483A, E484K/Q, F490S, S494L/P, N501Y are associated with immune escape.
SARS_CoV_2 mutation literature information.
PMID: 
2021
Antibody therapeutics
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