A fluorescence intensity plot for each treatment (e.g., +CCL2, +anti-CCL2, or +Isotype antibody control) for infection with each reporter virus (HIV-1IndieC1-mGL or HIV-1NLAD8-GFP-Nef) showed results consistent with the observation that the subtype C reporter is refractory to CCL2 levels, unlike the subtype B reporter virus (Figure 4D, compare left and right panels). This evidence concerns the gene S100B and infection.