DNA virus infections shape transposable element activity in vitro and in vivo [HFF]
We show strong activation of TEs in the context of DNA virus infection and investigate the molecular mechanisms of how TEs are induced. We demonstrate that herpesvirus infection leads to a robust expression of the MLT and THE1-class of LTR containing retrotransposons as well as a subset of long-interspersed nuclear elements-1 (LINEs), Alu-elements and some HERVs. Mechanistically we demonstrate that this TEs upregulation is induced by two pathways that act synergistically: de-repression of KAP1/TRIM28 mediated by phosphorylation and expression of the pioneer factor double-homeobox 4 (DUX4). Overall design: RNA-sequencing was performed from HCMV infection and KAP1 knockdown