FIG 4.
Inhibition and activation of HIV-1 infections by CCR5-derived proteins and peptides. (A) Comparison of Nt versus CCR5-IgG activation of HIV-1JRCSF(Ad) infections of HeLa-CD4/CCR5(Δ18) cells. Infectivity values were normalized relative to the infectivity obtained at 25 μM Nt. The results of a single experiment performed in duplicate are shown. A parallel study using an antibody-derived tyrosine-sulfated CCR5-mimetic IgG (30, 69) also showed no activation. (B) Comparison of CCR5-IgG inhibition of wild-type HIV-1JRCSF and HIV-1JRCSF(Ad) on JC.53 cells expressing wild-type CCR5. Relative infectivity values were generated by dividing the titers obtained at each concentration by the titers obtained in the absence of CCR5-IgG. The results of a representative experiment of two performed in duplicate are shown. (C) Nt inhibition of wild-type HIV-1JRCSF and HIV-1JRCSF(Ad) on JC.53 cells. Relative infectivity values were calculated by normalizing the titers obtained at each peptide concentration to the titers obtained on cells expressing wild-type CCR5 in the absence of Nt. Nt effectiveness was confirmed by its ability to activate HIV-1JRCSF(Ad) infections of HeLa-CD4/CCR5(Δ18) cells. The results of a representative experiment of two performed in duplicate are shown. All graphs were created with Microsoft Excel software (version 11.5.5).