A non-ACE2 competing human single-domain antibody confers broad neutralization against SARS-CoV-2 and circulating variants.
PMID: 34732694
2021
Signal transduction and targeted therapy
Result: We investigated several RBD variants within publicly available SARS-CoV-2 sequences in the Global Initiative on Sharing All Influenza Data (GISAID) and all of the individual RBD mutants (N501Y, E484K, E484Q, K417N, K417T, L452R, L452Q, T478K) found in dominant VOCs (B.1.1.7, Alpha; B.1.352, Beta; P.1, Gamma; B.1.617.2, Delta; B.1.427/B.1.429, Epsilon) for n3113.1 binding.
Method: They are: S.K417T.AAG.ACG, S.D614G.GAT.GGT, S.E484K.GAA.AAA, S.E484Q.GAA.CA
Result: Out of nine samples, five were B.1.617.2 (Delta) and concordant with sequencing showing mutation in D614G, L452R, P681R, and T478K, two samples were B.1.1.7 (Alpha) showing mutation in D614G, N501Y, delH69V70, Q27stop, and two were B.1.526 (Iota) showing mutation in L452R and D614G (Supplementary Material S5).
Molecular strategies for antibody binding and escape of SARS-CoV-2 and its mutations.
Discussion: On the other hand, for MT2, MT3, and RBD versions involving mutations K417N, L452R, E484K, T478K, and N501Y, the binding energy increased compared to the WT.
Discussion: We found that mutation N501Y marginally enhanced the binding energy between RBD and ACE2, while mutations MT2 (E484K/
Discussion: reported that the binding between SARS2 and ACE2 increases when the following mutations K417N, E484K, L452R, T478K, and N501Y are present, in good agreement with our findings.
Host Response to SARS-CoV2 and Emerging Variants in Pre-Existing Liver and Gastrointestinal Diseases.
PMID: 34760721
2021
Frontiers in cellular and infection microbiology
Abstract: The mutations in the spike protein of VOC are implicated for increased receptor binding (N501Y, P681R) and immune escape (L452R, E484K/Q, T478K/R) to host response.
Introduction: As of May 2021, three sublineages have been detected for this variant (B.1.617.1/2/3) with B.1.617.2 being the most dominant, having a unique T478K mutation absent in sublineages 1 and 3, serving as a possible route of immune evasion.
Postvaccination SARS-COV-2 among Health Care Workers in New Jersey: A Genomic Epidemiological Study.
Method: The SARS-CoV-2 target sequences include (i) the wild-type (WT) gene fragment of S protein (S; nucleotides [nt] 21,563 to 25,384; GenBank accession number MN908947); (ii) the mutant gene fragments of S protein, inclu
Table: T478K
Discussion: In our study, we developed a CRISPR-Cas12a-based genotyping assay and have approved its feasibility to detect single nucleotide mutations and to distinguish variants of SARS-CoV-2 based on the combination of a series of crRNAs that are specific for the most important and signature mutations, including K417N, L452R/Q, T478K, E484K/Q, and N501Y within the spike protein of SARS-CoV-2.
SARS-COV-2 Delta variant displays moderate resistance to neutralizing antibodies and spike protein properties of higher soluble ACE2 sensitivity, enhanced cleavage and fusogenic activity.
Abstract: The spike proteins of B.1.617.1, B.1.617.2, and AY.1 variants have several substitutions in the receptor binding domain (RBD), including L452R+E484Q, L452R+T478K, and K417N+L452R+T478K, respectively, that could potentially reduce effectiveness of therapeutic antibodies and current vaccines.
Linked nosocomial COVID-19 outbreak in three facilities for people with intellectual and developmental disabilities due to SARS-CoV-2 variant B.1.1.519 with spike mutation T478K in the Netherlands.
Abstract: Recently, SARS-CoV-2 delta variant prevails over different countries that have 3 unique mutation sites: E156del/R158G in the N-terminal domain and T478K in a crucial receptor binding domain.
Conclusion: It is great period to prepare a vaccine or a neutralizing antibody against SARS-CoV-2 delta variant to prevent another wave of SARS-CoV-2 pandemic although there is no experimental evidence to confirm the significance of the T478K mutation in the SARS-CoV-2 delta variant.
Conclusion: The analysis of mutation sites in the critical RBM of spike protein on the SARS-CoV-2 variants ascertained a distinct T478K mutation in the SARS-CoV-2 delta variant.
Table: T478K
Figure: The unique
Introduction and rapid dissemination of SARS-CoV-2 Gamma Variant of Concern in Venezuela.
PMID: 34800714
2021
Infection, genetics and evolution
Introduction: Delta VOC harbors several mutations, such as L452R and T478K, being the former associated with an increased transmission potential and reduced susceptibility to protective immunity, both at humoral and cellular level.
Mutation-Induced Long-Range Allosteric Interactions in the Spike Protein Determine the Infectivity of SARS-CoV-2 Emerging Variants.
Abstract: To address this question, here we have individually assessed the effects of SARS-CoV-2 variant-specific spike (S) protein receptor-binding domain (RBD
Introduction: Here, we have considered prominent spike receptor-binding domain (RBD) mutations that are commonly observed among the VOI/VOC variants (Table 1), namely, E484K, K417N, L452Q, L452R, N501Y, and T478K.
Introduction: Of these, T478K and K417N substitutions in the spike protein make it characteristically different from other VOIs.
SARS_CoV_2 mutation literature information.
PMID: 
2021
Signal transduction and targeted therapy
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