Again, we observed that prestimulation of resting CD4 T cells with either soluble LFA-3 or the anti-CD2 antibody blocked HIV-1 latent infection (Figures 1I, 1J, and S4), demonstrating that the anti-HIV activity from CD2 prestimulation did not result from possible peculiarities of the anti-CD2 antibody, but likely from intracellular signaling events initiated from CD2 binding by LFA-3 or the anti-CD2 antibody. Here, CD58 is linked to disease arising from reactivation of latent virus.