No Higher Infectivity But Immune Escape of SARS-CoV-2 501Y.V2 Variants

TLDR: The data suggest that the enhancement of infectivity in mouse may lead to the spillover of 501Y.V2 to mouse, which may compromise the efficacy of monoclonal antibodies, convalescent sera and vaccines.

Abstract: The 501Y.V2 variants contain multiple mutations in the spike region. We found that they had no significant increased effect on infectivity to human cell lines and cells overexpressing human ACE2, but increased infectivity in cells overexpressing mouse ACE2 based on the pseudotyped viruses. The susceptibility of 501Y.V2 variants to many neutralizing monoclonal antibodies decreased significantly. These variants also had a significant reduced effect on the neutralization ability of convalescent and RBD protein immunized sera. The immune resistances were mainly caused by E484K and N501Y mutations located in receptor binding region. These data suggest that the enhancement of infectivity in mouse may lead to the spillover of 501Y.V2 to mouse. The immune resistance of 501Y.V2 may compromise the efficacy of monoclonal antibodies, convalescent sera and vaccines. Funding: This work was supported by General Program ofNational Natural Science Foundation of China [grant number 82073621], BILL & MELINDA GATES FOUNDATION [Investment ID INV-006379], National Science and Technology Major Projects of Drug Discovery [grant number 2018ZX09101001] and National Science and Technology Major Projects of Infectious Disease [grant number 2017ZX10304402]. Conflict of Interest: All the authors declare no competing interests. Ethical Approval: The protocol of the animal study was approved by Ethical review Committee for Animal Welfare of The National Institutes for Food and Drug Control.