Our data supports this hypothesis as we observed elevated class-switching during KSHV reactivation (Figure 1D), upon low levels of de novo infection resulting in vIL-6 and K8.1 gene expression (Figures 1B, 3A), and with vIL-6 lentiviral transduction in B cells (Figures 3C,D), implying that KSHV replication and paracrine signaling may contribute to this process. Here, KRT81 is linked to infection.