FIG. 6.
Epitope specificity of neutralization of HIV-2KR.X7/HIV-1 V3 chimeras by HIV-1 subtypes B and C plasmas. (A) Neutralization of HIV-2KR.X7/HIV-1 YU2 and Ccon V3 chimeras but not parental HIV-2 strains by plasma from subjects infected by HIV-1 subtype B and C. Neutralization of the HIV-2KR.X7 YU2 V3 chimera by HIV-1 clade B plasma is inhibited modestly by the V3JR-FL 24-mer peptide (B) and nearly completely by Fc-V3B FP (C, left). Neutralization of the HIV-2KR.X7 YU2 V3 chimera by HIV-1 clade C plasma is inhibited equally by Fc-V3B FP and Fc-V3C FP (C, right). V3 peptides and fusion protein (FP) competitors are shown in Table 2. For all experiments, fivefold serial dilutions of plasma were combined with peptide or fusion protein and incubated at 37°C for 30 min. Virus was then added and incubated at 37°C for 1 h, and the mixture transferred to TZM-bl reporter cells. The final peptide and fusion protein concentrations in all wells were 50 μg/ml and 10 μg/ml, respectively. Luciferase expression was assessed 48 h later and was normalized to that in the absence of plasma or inhibitor. Scrambled (scr) V3 peptide, fusion proteins lacking complete or partial V3 sequences, and medium-only controls had no effect on virus neutralization.