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. Author manuscript; available in PMC: 2018 Nov 10.
Published in final edited form as: Oncogene. 2018 May 10;37(33):4534–4545. doi: 10.1038/s41388-018-0282-4

Figure 1. KSHV de novo infection or viral latent proteins transactivate HERV-K in vitro and in vivo.

Figure 1

(A) Human umbilical vein endothelial cells (HUVEC) were infected with purified KSHV (MOI~10) or UV-inactivated KSHV for 2h, then the induction of HERV-K reactivation at indicated time-points post-infection (p.i.) was measured and compared to UV-inactivated KSHV infected cells control by qRT-PCR with the specific primers for HERV-K env gene. (B) The levels of HERV-K transactivation within peripheral blood mononuclear cells (PBMCs) from HIV+ patients with or without KSHV co-infection were quantified using qRT-PCR. KSHV infection status was identified using ELISA as described in the Methods. (C) HUVEC were infected by purified KSHV as described above, then the transcripts of viral latent genes Lana (Orf73) and vFlip (Orf71) at indicated time-points p.i. were measured and compared to control mock cells by using qRT-PCR. (D-F) HUVEC were transfected with control vector (pc) or vectors encoding LANA (pcLANA), vFLIP (pcvFLIP) or RTA (pcRTA) at 0.2, 1.0 or 2.5 μg, respectively, for 48 h, then the induction of HERV-K transactivation was quantified by using qRT-PCR. Error bars represent the S.D. from 3 independent experiments. * = p<0.05, ** = p<0.01.