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. Author manuscript; available in PMC: 2015 May 6.
Published in final edited form as: Nature. 2014 Sep 3;515(7525):138–142. doi: 10.1038/nature13601

Figure 2. Binding specificity of 35O22.

Figure 2

a, Neutralization of HIVJRCSF pseudovirus or variants containing the indicated mutations. b, Binding to BG505 SOSIP.664 trimer produced in cells treated with kifunensine or deficient in glycan processing (293S). c, Binding to BG505 trimers with the indicated mutations. BG505 SOSIP.SEKS lacks the furin cleavage site. BG505 WT.664 lacks stabilizing mutations and the antigen primarily represents gp41. d, SPR analysis of binding to immobilized BG505 SOSIP.664 trimers. e, Binding of 35022 (250 nM) to BG505 SOSIP.664 trimers, gp120-gp41ECTO protomers, or monomeric gp120. f, Binding to BG505 SOSIP.664, BG505 SOSIP.SEKS, or the BG505 WT.SEKS lacking the SOSIP mutations.