Abstract
SummaryThe 501Y.V2 variants of SARS-CoV-2 containing multiple mutations in spike are now dominant in South Africa and are rapidly spreading to other countries. Here, experiments with 18 pseudotyped viruses showed that the 501Y.V2 variants do not confer increased infectivity in multiple cell types except for murine ACE2-overexpressing cells, where a substantial increase in infectivity was observed. Notably, the susceptibility of the 501Y.V2 variants to 12 of 17 neutralizing monoclonal antibodies was substantially diminished, and the neutralization ability of the sera from convalescent patients and immunized mice was also reduced for these variants. The neutralization resistance was mainly caused by E484K and N501Y mutations in the receptor-binding domain of spike. The enhanced infectivity in murine ACE2-overexpressing cells suggests the possibility of spillover of the 501Y.V2 variants to mice. Moreover, the neutralization resistance we detected for the 501Y.V2 variants suggests the potential for compromised efficacy of monoclonal antibodies and vaccines.
Highlights
As of early February 2021, SARS-CoV-2 had infected more than 100 million people worldwide and killed more than 2 million people
SARS-CoV-2 is a member of the coronavirus family, which carries the largest genome among single-stranded RNA viruses
It is clear that the SARSCoV-2 RBD is an essential region for virus binding to the cell receptor ACE2 (Barnes et al, 2020; Hoffmann et al, 2020; Lan et al, 2020; Shang et al, 2020; Walls et al, 2020), and the RBD is a dominant immune epitope of the S protein (Baum et al, 2020; Brouwer et al, 2020; Cao et al, 2020; Lv et al, 2020; Shi et al, 2020; Wu et al, 2020). 501Y.V2-3, which has three mutated amino acids in its RBD, is one of the most complicated SARS-CoV-2 variants detected to date (Tegally et al, 2020a)
Summary
As of early February 2021, SARS-CoV-2 had infected more than 100 million people worldwide and killed more than 2 million people (https://covid19.who.int). The D614G mutation in the S protein increases viral infectivity in susceptible cells by 8- to 10-fold (Li et al, 2020; Zhang et al, 2020), and both the infectivity and transmissibility of the D614G mutant virus are significantly elevated in a hamster model (Hou et al, 2020; Plante et al, 2020). This may at least partially explain how the 614G virus spread so rapidly; 614G overtook the 614D virus within 3 months of its emergence in February 2020 (Korber et al, 2020)
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