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. 2012 Apr;86(8):4404–4419. doi: 10.1128/JVI.06617-11

Fig 5.

Fig 5

Effects of TPA, apoptosis triggered by DCPE, and induction of the ORF50ΔSTAD expression by a low concentration of DOX on KSHV DNA and virion production in BCBL-1 cells and ORF50ΔSTAD BCBL-1 cells. BCBL-1 and ORF50ΔSTAD BCBL-1 cells were subjected to several treatments: TPA to induce FL ORF50 expression and viral replication via the normal pathway, DOX (a low concentration of 0.1 μg/ml) to induce ORF50ΔSTAD expression, and DCPE to induce apoptosis, and combinations of the agents. Production of total and protected KSHV DNA was measured using a real-time PCR assay (25). (A) KSHV total DNA in BCBL-1 cells. (B) KSHV total DNA in ORF50ΔSTAD BCBL-1 cells. (C) KSHV virion protected DNA in BCBL-1 cells. (D) KSHV virion protected DNA in ORF50ΔSTAD BCBL-1 cells. (E) Effects of low concentrations of DOX on KSHV replication in ORF50ΔSTAD BCBL-1 cells. The levels of ORF50ΔSTAD induced by very low concentrations of DOX (0.001 μg/ml) completely suppress KSHV replication induced by TPA. (The levels of KSHV replication are below the baseline level for samples from cells treated with a low concentration of DOX, because ORF50ΔSTAD blocks the small amount of spontaneous KSHV replication that occurs in the cells.) TPA induces KSHV replication, and TPA-induced KSHV replication is blocked by ORF50ΔSTAD. DCPE also induces KSHV replication, but DCPE-induced KSHV replication is not blocked by ORF50ΔSTAD.