SARS_CoV_2 mutation literature information.


  Molecular rationale for SARS-CoV-2 spike circulating mutations able to escape bamlanivimab and etesevimab monoclonal antibodies.
 PMID: 34642465       2021       Scientific reports
Abstract: The main findings from this study show that, compared to the wild-type SARS-CoV-2 spike protein, mutations E484A/G/K/Q/R/V, Q493K/L/R, S494A/P/R, L452R and F490S are predicted to be markedly resistant to neutralization by LY-CoV555, while mutations K417E/N/T, D420A/G/N, N460I/K/S/T, T415P, and Y489C/S are predicted to confer LY-CoV016 escaping advantage to the viral protein.
Result: 5D):the DeltaDeltaG values currently predicted for replacement of both these spike


  Global Prevalence of Adaptive and Prolonged Infections' Mutations in the Receptor-Binding Domain of the SARS-CoV-2 Spike Protein.
 PMID: 34696404       2021       Viruses
Abstract: In the case of prolonged infections' mutations (long-term SARS-CoV-2 infections), V483A (0.009%) was found to be dominant followed by Q493R (0.009%), while other mutations were found in less than 0.007% of the studied sequences.
Result: As mentioned before, the Q493R mutation alone confers significant resistance towards bamlanivimab, etesevimab, casirivimab and C144.
Result: During this period, the prevalence of Q493R, Q493K, E484A and T470N increased by 0.004, 0.001, 0.003 and 0.001% points, respectively, while the prevalence of V483A and T415A decreased by 0.01 and 0.005% points, respectively.


  Emergence of SARS-CoV-2 resistance mutations in a patient who received anti-SARS-COV2 spike protein monoclonal antibodies: a case report.
 PMID: 34876033       2021       BMC infectious diseases
Abstract: CASE PRESENTATION: We here report the case of an immunosuppressed patient infected with a B.1.1.7 variant, who received a combination of monoclonal antibodies, and subsequently selected mutations K417N, E484K and Q493R on Spike protein of SARS-CoV-2.
Conclusion: It showed a typical B1.1.7 variant on the first sample (April 13th); double populations: K417K/N, E484E/K and Q493Q/R on the 2nd sample (28th April), and E484K and K417N on the 3rd sample (May 8th).
Discussion: Other mutations on the S protein liable to escape mAbs effect have been described, especially K417N and <


  Structural models of SARS-CoV-2 Omicron variant in complex with ACE2 receptor or antibodies suggest altered binding interfaces.
 PMID: 34931193       2021       bioRxiv
Result: Conversely, Q493R permits the formation of two backbone hydrogen bonds.
Result: Finally, Q493R led to a 70-fold reduction in REGN10933 binding.
Result: Furthermore, three of four models highlight the energetic unfavorability of Q493R for binding, which may result in the loss of two hydrogen bonds.


  Booster of mRNA-1273 Strengthens SARS-CoV-2 Omicron Neutralization.
 PMID: 34931200       2021       medRxiv
Introduction: The Omicron spike in this study contained mutations A67V, Delta69-70, T95I, G142D, Delta143-145, Delta211, L212I, +214EPE, G339D, S371L, S373P, S375F, K417N, N440K, G446S, S477N, T478K, E484A, Q493R, G496S, Q498R, N501Y, Y505H, T547K,


  SARS-CoV-2 Omicron neutralization by therapeutic antibodies, convalescent sera, and post-mRNA vaccine booster.
 PMID: 34981057       2021       bioRxiv
Introduction: The predominant strain of Omicron has mutations in the spike gene encoding 15 amino acid changes in the receptor binding domain (RBD) of the spike surface protein (G339D, S371L, S373P, S375F, K417N, N440K, G446S, S477N, T478K, E484A, Q493R, G496S, Q498R, N501Y, and Y505H).


  Analysis of Immune Escape Variants from Antibody-Based Therapeutics against COVID-19: A Systematic Review.
 PMID: 35008446       2021       International journal of molecular sciences
Abstract: While the former is mainly associated with specific single amino acid mutations at residues within the receptor-binding domain (e.g., E484K/Q, Q493R, and S494P), a few cases of immune evasion after CCP were associated with recurrent deletions within the N-terminal domain of the spike protein (e.g., DeltaHV69-70, DeltaLGVY141-144 and DeltaAL243-244).
Discussion: Similarly, Q493R, which causes resistance to bamlanivimab + etesevimab, had only been reported in 244 sequences and Q493K in 138 sequences, before becoming one of the hallmark mutations of VOC Omicron.



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