In order to present more physiologically relevant studies, an over-the-counter resveratrol dietary supplement (RDS) was used to treat KSHV-infected BCBL-1 cells under TPA-induced conditions. RDS containing 100 mM resveratrol did not significantly induce cell death as monitored by the lactate dehydrogenase assay (data not shown). These results were confirmed by the conventional trypan blue test. More than 95% of the target cells were found to be viable when the target cells were treated with RDS (data not shown). As shown in earlier reports [12] , TPA treatment augments phospho-ERK1/2 expression (Fig. 6A, lane 2) . The effect of TPA also resulted in an increase in Egr-1 and KSHV RTA expression when compared to uninduced cells (Fig. 6A, lane  2) . Unfiltered RDS successfully inhibited phospho-ERK1/2, Egr-1, and RTA expression in TPA-induced KSHV-infected cells (Fig. 6A, lane 3) . A slightly lesser inhibitory effect was observed in cells that were treated with RDS that had particulates removed using a 0.2 mm filter (Fig. 6A, lane 4) . We did not discover either form of RDS to have noticeable effect on endogenous ERK1/2 and actin controls (Fig. 6A, lanes 3 and 4) . The data from Western blotting (Fig. 6A ) was further confirmed in HEK293 cells by IFA (Fig. 6B) . To authenticate the results from monitoring the effect of RDS on protein levels of Egr-1 and RTA, we analyzed the effect of RDS on (i) uninduced cells transfected with vectors encoding egr-1, and (ii) TPA-induced KSHV reactivation in BCBL-1 cells by performing qRT-PCR. Our results clearly demonstrate the ability of RDS to lower the expression of both egr-1 and ORF50 under both circumstances (Fig. 6C, D) . Finally, ChIP assay was performed to discern the specificity of RDS on virus reactivation using primers specific to ORF50P8 region. Under TPA-induced conditions, Egr-1 specifically targeted ORF50P8 (Fig. 6E . cycles 25 and 30). However, under RDS treated conditions the binding of Egr-1 to ORF50P8 was significantly decreased (Fig. 6E, cycles 25  and 30 ). For negative controls, samples were IP with (NS) IgGs and recruitment of Egr-1 to ORF50P was not observed (Fig. 6E) . However, positive controls using specific Abs to histone proteins recovered ORF50P targets (Fig. 6E) . These results suggest resveratrol in its chemical form and RDS may lower Egr-1 expression to inhibit KSHV reactivation from latency.