ACE2 host variant dependency
- This mutation's measured interaction affinity with ACE2:p.S19P (0.03% minor allele frequency, found almost exclusively in African/African-Americans in the GnomAD database) was significantly lower than the predicted value, indicating that these mutations were not independent. This is consistent with the fact that the ACE2 residue S19 is adjacent to RBD residue S477 in the contact interface.
(Barton et al. (2021))
ACE2 receptor binding affinity
- Experimentally, ACE2 binding affinity increased 0.06 fold (Starr et al. (2020))
- Increased affinity for ACE2: clade in Australia 2020-05-27 onward, clade in Europe 2020-08-08 onward.
Modelling shows flexible region in Spike RBD with residue S477 having the greatest rotational flexibility. https://assets.researchsquare.com/files/rs-106969/v2_stamped.pdf (Starr et al. (2020))
- Among the first selected minor variants in an in vitro evolution experiment for ACE2 binding, with increasing proportion in subsequent rounds.
(Zahradnik et al. (2021))
Antibody epitope effects
- Mutant screen in neutralization assay with a broad range of monoclonal antibodies shows some resistence across all antibodies tested.
(Liu et al. (2021))
- Ablates binding by class 3 mAbs such as C135 that do not directly interfere with ACE2 binding, but clonal somatic mutations of memory B cells at 6.2 months (evolving humoral immune response) show pronounced increase in binding to the variant.
(Gaebler et al. (2021))
Convalescent plasma escape
- Mixed bag of mild positive and negative changes in neutralization capability of all 4 convalescent sera tested.
Against a wider panel of 16 convalescent plasma (no replicates), 10 show low neutralization. (Liu et al. (2021))
- Estimated free energy change (ddG) for this variant is 0.22 kcal/mol (i.e. stabilizing relative to wild type) (Spratt et al. (2021))
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