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This is a PDF file of a peer-reviewed paper that has been accepted for publication. Although unedited, the content has been subjected to preliminary formatting. Nature is providing this early version of the typeset paper as a service to our authors and readers. The text and figures will undergo copyediting and a proof review before the paper is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers apply.

ARS-CoV-2 variants have rapidly emerged in humans and supplanted ancestral strains [1][2][3][4][5] . Their proposed increased rates of interindividual transmission conferred a replication advantage at the population level. One of the first identified variants includes the D614G mutation in the gene encoding the spike (S) protein, which enhances viral infectivity and shifts S protein conformation toward an angiotensin-converting enzyme 2 (ACE2)-binding fusion-competent state, without significantly modifying sensitivity to antibody neutralization 1,6-8 . More recently, novel variants have appeared in multiple countries, with combinations of mutations and deletions in the receptor-binding domain (RBD) and N-terminal domain of S protein, as well as in other proteins. The B.1.1.7 variant emerged in the United Kingdom, the B.1.351 variant (also termed 501Y.V2) in South Africa and the P.1 and P.2 lineages in Brazil 2,3,5,9-12 . Although distinct, the variants share common characteristics, including known escape mutations that were previously identified under antibody pressure selection in vitro 2,3,[13][14][15][16][17] . Some of the mutations or deletions were also identified in immunocompromised individuals with prolonged infectious viral shedding and treated with convalescent plasma or S-protein Sensitivity of infectious SARS-CoV-2 B.1.1.7 and B.1.351 variants to neutralizing antibodies