To establish a critical role for these interactions between Egr-1 and ORF50P, luciferase reporter constructs were used to investigate the necessity of ORF50P3 and ORF50P8 during Egr-1-mediated activation of the ORF50P. Empty vector (pGL3) or vectors encoding a deletion series of ORF50P (Fig. 2B ) along with the downsteam luciferase gene were transiently transfected into target cells in conjunction with empty vector or egr-1/ pcDNA3.1(+). Cells transfected with pcDNA3.1(+) did not induce significant luciferase activity (Fig. 2C) . However, following incubation of cells transfected with egr-1/pcDNA3.1(+), we noticed the luciferase activity to be significantly greater in cells that were also transfected with constructs encoding the full length (FL) ORF50P compared to cells transfected with pGL3 ( Fig. 2C) , Furthermore, we observed a decrease in relative luciferase activity following deletion of the fragment containing the ORF50P3 domain (D-2922 to -2044; D-2922 to -1322; D-2922 to -894; and D-2922 to -169) when compared to the construct encoding full length ORF50P (Fig. 2C) . Although the absence of ORF50P3 contributed to a decrease in luciferase activity, this activity was never completely abolished ( Fig. 2C) suggesting the need for an intact ORF50P3 and ORF50P8 for an optimal Egr-1-induced transcription of ORF50. Taken together, these results suggest a role for Egr-1 to specifically bind and activate ORF50P to trigger a lytic infection in KSHV-infected cells.