Analysis of the ARTIC Version 3 and Version 4 SARS-CoV-2 Primers and Their Impact on the Detection of the G142D Amino Acid Substitution in the Spike Protein.
Introduction: In particular, there were spike protein amino acid changes common to the Beta, Delta, and Gamma variants that occurred in known V3 primer binding sites, including G142D (Delta) in the 2_Right primer, the 241/243del (Beta) that occurs in the 74_Left primer, and the K417N (Beta) or K417T (Gamma) which occur in the 76_Left primer (https://community.artic.network/t/sars-cov-2-version-4-scheme-release/312).
Emergence of novel combinations of SARS-CoV-2 spike receptor binding domain variants in Senegal.
Introduction: Subsequent reports have demonstrated that increased transmissibility and immune escape are linked to these lineages, which are defined by spike receptor binding domain (RBD) mutations, including N501Y, K417N/T, L452R, and E484K.
Additional Positive Electric Residues in the Crucial Spike Glycoprotein S Regions of the New SARS-CoV-2 Variants.
Abstract: Here, we developed five SARS-CoV-2 spike gene primer pairs (5-SSG primer assay; 69S, 144S, 417S, 484S, and 570S) and verified their ability to detect nine key spike mutations (DeltaH69/V70, T95I, G142D, DeltaY144, K417T/N, L452R, E484K/Q, N501Y, and H655Y) using a Sanger sequencing-based assay.
Insights on the mutational landscape of the SARS-CoV-2 Omicron variant.
Result: Further, we note the that Omicron mutations may also enhance escape depth from class 1 antibodies beyond that observed for the Beta variant due to accumulation of additional mutations in class 1 antibody epitopes beyond the shared Beta/Omicron mutation K417N.
Result: We find that Omicron has accumulated multiple tightly clustered mutations and therefore may have enhanced escape from matured polyclonal responses that are tolerant of certain class 1 antibody escape mutations such as K417N and N501Y (see Figure 1).
Loss of Neutralizing Antibody Response to mRNA Vaccination against SARS-CoV-2 Variants: Differing Kinetics and Strong Boosting by Breakthrough Infection.
Introduction: Another VOC to emerge at about the same time was Beta (B.1.351), which is characterized by other NTD mutations and deletions, as well as key RBD mutations, including K417N, E484K, and N501Y.
SARS-CoV-2 Omicron has extensive but incomplete escape of Pfizer BNT162b2 elicited neutralization and requires ACE2 for infection.
Method: P2 stock was sequenced and confirmed Omicron with the following substitutions: E:T9I,M:D3G,M:Q19E,M:A63T,N:P13L,N:R203K,N:G204R,ORF1a:K856R,ORF1a:L2084I,ORF1a:A2710T,ORF1a:T3255I,ORF1a:P3395H, PMID: 34912372
2021
Frontiers in genetics
Introduction: In December 2020, the variant B.1.351 was first detected in South Africa, with mutations such as K417N, E484K, N501Y, D614G, and A701V.
Structural analysis of receptor binding domain mutations in SARS-CoV-2 variants of concern that modulate ACE2 and antibody binding.
Introduction: The one RBD mutation occurring outside of the RBM, K417N/T, additionally exhibits ambiguity in mutation, with the P.1 strain mutated to threonine (K417T) and the B.1.351 strain mutated to asparagine (K417N) (Figure 1B).
Result: D614G + N501Y + E484K + K417T/N.
Result: Interestingly, the K417N mutation reduced ACE2 affinity to a greater extent than the K417T mutation (both in isolation and when combined with D614G + N510Y + E484K).
Result: Mutations at the 417 position ( PMID: 34923570
2021
Cell discovery
Method: pS-B.1.1.7 and pS-B.1.351 plasmids were constructed with mutant S genes expressing the spike protein of the B.1.1.7 variant (GenBank: QQH18545.1, containing the H69, V70, and Y145 deletions and N501Y, A570D, D614G, P681H, T716I, S982A, and D1118H mutations) and B.1.351 variant (GenBank: QRI43207.1, containing the L242, A243, and L244 deletions and L18F, D80A, D215G, S305T, K417N, E484K, N501Y, D614G
SARS_CoV_2 mutation literature information.
PMID: 
2021
Microbiology spectrum
Browser Board
Co-occurred Entities
Filtrator
ViMRT