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- W4220739320 endingPage "e202201415" @default.
- W4220739320 startingPage "e202201415" @default.
- W4220739320 abstract "Breakthrough infections by emerging SARS-CoV-2 variants raise significant concerns. Here, we sequence-characterized the spike gene from breakthrough infections that corresponded to B.1.617 sublineage. Delineating the functional impact of spike mutations revealed that N-terminal domain (NTD)-specific E156G/Δ157-158 contributed to increased infectivity and reduced sensitivity to vaccine-induced antibodies. A six-nucleotide deletion (467-472) in the spike-coding region introduced this change in the NTD. We confirmed the presence of E156G/Δ157-158 from cases concurrently screened, in addition to other circulating spike (S1) mutations such as T19R, T95I, L452R, E484Q, and D614G. Notably, E156G/Δ157-158 was present in more than 90% of the sequences reported from the USA and UK in October 2021. The spike-pseudotyped viruses bearing a combination of E156G/Δ157-158 and L452R exhibited higher infectivity and reduced sensitivity to neutralization. Notwithstanding, the post-recovery plasma robustly neutralized viral particles bearing the mutant spike. When the spike harbored E156G/Δ157-158 along with L452R and E484Q, increased cell-to-cell fusion was also observed, suggesting a combinatorial effect of these mutations. Our study underscores the importance of non-RBD changes in determining infectivity and immune escape." @default.
- W4220739320 created "2022-04-03" @default.
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- W4220739320 date "2022-03-16" @default.
- W4220739320 modified "2023-10-11" @default.
- W4220739320 title "SARS-CoV-2 spike E156G/Δ157-158 mutations contribute to increased infectivity and immune escape" @default.
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- W4220739320 doi "https://doi.org/10.26508/lsa.202201415" @default.
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