Abstract:
SARS-CoV-2 has caused the COVID-19 pandemic. Recently, B.1.617 variants have been transmitted rapidly in India. The transmissibility, pathogenicity, and neutralization characteristics of these variants have received considerable interest. In this study, 22 pseudotyped viruses were constructed for B.1.617 variants, as well as 16 corresponding single amino acid mutations. B.1.617 variants did not exhibit enhanced infectivity in humans, but mutations T478K and E484Q in the RBD led to enhanced infectivity in mouse ACE2-overexpressing cells. Furin a (...)
SARS-CoV-2 has caused the COVID-19 pandemic. Recently, B.1.617 variants have been transmitted rapidly in India. The transmissibility, pathogenicity, and neutralization characteristics of these variants have received considerable interest. In this study, 22 pseudotyped viruses were constructed for B.1.617 variants, as well as 16 corresponding single amino acid mutations. B.1.617 variants did not exhibit enhanced infectivity in humans, but mutations T478K and E484Q in the RBD led to enhanced infectivity in mouse ACE2-overexpressing cells. Furin activities were slightly increased against B.1.617 variants and cell–cell fusion was also enhanced. Furthermore, B.1.617 variants escaped neutralization by several mAbs, mainly because of mutations L452R, T478K, and E484Q in the RBD. The neutralization activities of sera from convalescent patients, inactivated vaccine, or adenovirus vaccine-immunized volunteers; and SARS-CoV-2 immunized animals against pseudotyped B.1.617 variants were reduced by about two-fold compared with the D614G virus. (Read More)
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