A/Hong Kong/1/1968 mutant T32I, = 2.3 nM Kd A/Hong Kong/1/1968 mutant T32R, = 19 nM Kd A/Hong Kong/1/1968 mutant Q34T, = 120 nM Kd A/Hong Kong/1/1968 mutant Q34R, = 350 nM Kd A/Hong Kong/1/1968 mutant L38Y, = 0.9 nM Kd A/Victoria/3/1975 (H3N2), = 0.5 nM Kd A/Leningrad/360/1986 (H3N2), = 1.3 nM Kd A/Beijing/353/1989 (H3N2), = 2.6 nM Kd A/Shangdong/9/1993 (H3N2), = 0.4 nM Kd A/Moscow/10/1999 (H3N2), = 6.4 nM Kd A/Panama/2007/1999 (H3N2), = 5.4 nM Kd data were fit with a 2:1 binding model, yielding apparent = 5.4 nM and = 190 nM. Kd1 Kd2 The dominant binding process (accounting for the majority of the shift in observed wavelength) corresponds to the higher affinity process (Kd1 = 5.4 nM). The lower affinity process may reflect a non-specific interaction. Therefore, we report the affinity for this interaction as 5.4 nM in Figure 2. A/Brisbane/10/2007 (H3N2), = 0.7 nM Kd
A/Hong Kong/1/1968 mutant T32I, Kd = 2.3 nM A/Hong Kong/1/1968 mutant T32R, Kd = 19 nM A/Hong Kong/1/1968 mutant Q34T, Kd = 120 nM A/Hong Kong/1/1968 mutant Q34R, Kd = 350 nM A/Hong Kong/1/1968 mutant L38Y, Kd = 0.9 nM A/Victoria/3/1975 (H3N2), Kd = 0.5 nM A/Leningrad/360/1986 (H3N2), Kd = 1.3 nM A/Beijing/353/1989 (H3N2), Kd = 2.6 nM A/Shangdong/9/1993 (H3N2), Kd = 0.4 nM A/Moscow/10/1999 (H3N2), Kd = 6.4 nM A/Panama/2007/1999 (H3N2), Kd = 5.4 nM data were fit with a 2:1 binding model, yielding apparent Kd1 = 5.4 nM and Kd2 = 190 nM. The dominant binding process (accounting for the majority of the shift in observed wavelength) corresponds to the higher affinity process (Kd1 = 5.4 nM). The lower affinity process may reflect a non-specific interaction. Therefore, we report the affinity for this interaction as 5.4 nM in Figure 2. A/Brisbane/10/2007 (H3N2), Kd = 0.7 nM