Glycoprotein 120–mimic peptides inhibit HIV-1 entry and spreading. (A) Inhibition of basal infection by gp120-mimic peptides. PBMCs were infected with either IIIB(F = 268.78; *P ≤ .05 versus the lowest concentration of each peptide) or Ba-L (F = 175.54; *P ≤ .05). (B) Inhibition of Tat-promoted infection by gp120-mimic peptides. PBMCs were treated with rTat and infected with III B (F = 156.73; P ≤ .05) or Ba-L (F = 160.73; P ≤ .05). In panels A and B, percent inhibition of virus entry was evaluated as described in the legend to Figure 4A, compared with respective control infections; peptide concentrations were as follows: CT303 and CT304, 100 to 50 to 10 μM; CT319, 1 μM to 100 to 10 nM. (C) CT319 reverts Tat-induced spreading of the infection. PBMCs were infected with either III B or Ba-L in presence of rTat (as shown in Figure 4) and 1 nM CT319 (▴) or GACVRLSACGA control peptide (▪). (D) CT319 exhibits a dose-dependent inhibitory effect on HIV-1 spreading. PBMCs were infected with III B or Ba-L and treated every 72 hours with the indicated amounts of CT319 (▴, 1 nM; +, 10 nM) or with 10 nM GACVRLSACGA control peptide (▪; III B, F = 124.3; Ba-L, F = 418.6; *P ≤ .005 within CT319-treated and control cells, §P ≤ .005 versus the lowest peptide concentration tested). (E) Single peptide administrations have different outcomes on the spreading of the infection. PBMCs were infected with III B, and 1 nM CT319 (▴) or GACVRLSACGA control peptide (▪) was administered at the indicated time points (III B, F = 219.8; Ba-L, F = 818.2; *P ≤ .005 within CT319-treated and control cells). Similar results were obtained for Ba-L infection. Each value indicates mean ± SD of 3 experiments performed in triplicate.