DNA virus infections shape transposable element activity in vitro and in vivo (HCMV,KSHV,DUX4)
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,KSHV infection and DUX OE; CUT&RUN was performed from HSV-1 infection.