Fig. 2. Schematic diagram of potential mechanisms for KSHV promoting HERV transactivation.

During KSHV de novo infection, LANA induces env transcripts through enhancing ERK activity, and vFLIP induces env transcripts through activating NF-κB activity. Np9 expression mediated by KSHV can promote virus-induced anchorage-independent growth (AIG) and invasion through the CD147-ADAMTS1/ADAMTS9-VEGF/VEGFR1 axis. LANA: a latency-associated nuclear antigen; vFLIP: viral FADD-like interleukin-1-β-converting enzyme (FLICE)/caspase-8-inhibitory protein; ERK: extracellular-signal-regulated kinase; ADAMTS1: a disintegrin and metalloproteinase with thrombospondin motifs 1; ADAMTS9: a disintegrin and metalloproteinase with thrombospondin motifs 9; VEGF: vascular endothelial growth factor; VEGFR1: vascular endothelial growth factor receptor 1