Although the transcription factor NFAT5 binds to a core NF-κB binding motif in the HIV-1 LTR enhancer region of subtype B, when two thymines (TT) are changed to cytosines (CC) in the proximal NF-κB binding motif (named N5-Mut) (bottom of Figure 1B), the binding of NFAT5 can be disrupted while leaving binding of NF-κB unperturbed [31]. We examined the requirement of NFAT5 for MTb-induced LTR activity by transfecting a wild-type and NFAT5 mutant LTR reporter construct into THP-1 cells, followed by stimulation with an MTb lysate. As shown in Figure 1B, in the absence of MTb lysate stimulation the activity of the NFAT5 binding site-mutant LTR was significantly reduced (p<0.05) in comparison to the wild-type LTR. When the NFAT5 binding site-mutant LTR was examined in THP-1 cells stimulated with the MTb lysate, its activity was reduced to an even more significant extent (p<0.01).