All that will do is select for B.1.351 to eventually become the dominant strain... although, they conveniently didn't have much to say regarding P.1 / Manaus. Additionally, there's plenty of B.1.351 floating around, find it hard to believe that nobody could get their hands on any... Somehow they felt compelled to pursue recombination with a Jan 2020 strain. Don't look behind that curtain.

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we engineered S mutations from the B.1.351 lineage into USA-WA1/2020, a relatively early isolate of the virus (in January 2020) (Fig. S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). We subsequently produced three recombinant viruses. The first had an N-terminal domain deletion and the globally dominant D614G substitution (Δ242-244+D614G),2,3 the second had mutations affecting three amino acids at the receptor-binding site (K417N, E484K, and N501Y) and a D614G substitution (B.1.351-RBD+D614G), and the third had all the mutations found in the S gene in the B.1.351 lineage (B.1.351-spike). All the mutant viruses yielded infectious titers exceeding 107 plaque-forming units per milliliter. The B.1.351-spike virus formed plaques that were smaller than those of the other viruses (Fig. S2).

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We performed 50% plaque reduction neutralization testing (PRNT50) using 20 serum samples that had been obtained from 15 participants in the pivotal trial1,4 2 or 4 weeks after the administration of boost immunization with 30 μg of BNT162b2 (which occurred 3 weeks after the first immunization) (Fig. S3). All the serum samples neutralized USA-WA1/2020 and all mutant viruses at titers of 1:40 or greater. Geometric mean neutralizing titers against USA-WA1/2020, Δ242-244+D614G, B.1.351-RBD+D614G, and B.1.351-spike viruses were 501, 485, 331, and 184, respectively (Figure 1 and Table S1). Thus, as compared with neutralization of USA-WA1/2020, neutralization of Δ242-244+D614G virus was similar and neutralization of the B.1.351-spike virus was weaker by approximately two thirds. Our data are also consistent with poorer neutralization of the virus with the full set of B.1.351-spike mutations than virus with either subset of mutations and suggested that virus with mutant residues in the receptor-binding site (K417N, E484K, and N501Y) is more poorly neutralized than virus with Δ242-244, which is located in the N-terminal domain of the spike protein.

Limitations of the study include a lack of systematic examination of individual mutations and the potential for mutations to alter neutralization by affecting spike function rather than antigenicity. The onset of protection after one dose of BNT162b2 precedes the development of high neutralizing titers, and BNT162b2 immunization also elicits CD8+ T-cell responses.1,4,5 Thus, it is unclear what effect a reduction in neutralization by approximately two thirds would have on BNT162b2-elicited protection from Covid-19 caused by the B.1.351 lineage of SARS-CoV-2.

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