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. 2020 Jun 12;18(10):559–570. doi: 10.1038/s41579-020-0382-3

Fig. 2. Viral strategies to avoid epigenetic repression.

Fig. 2

Viruses can counteract epigenetic repression in multiple ways in order to enrich for histones bearing active marks (shown as green histones with H3Ac, H4Ac and H3K4me3 marks) and prevent the loading of histones with repressive marks (red histone variant H3.3 bearing the repressive mark H3K9me3). a | The herpes simplex virus 1 (HSV-1) protein VP16 associates with the host factors HCF-1 and Oct-1, with HCF-1 recruiting the host H3K9 demethylases LSD1 and JMJD2 to remove repressive marks, along with the H3K4 methyltransferases Set1 and MLL1 to deposit active marks on viral DNA. b | Several viral proteins target pro-myelocytic leukaemia nuclear body (PML-NB) components in order to avoid epigenetic repression. HSV-1 ICP0 and human cytomegalovirus (HCMV) IE1 induce the degradation of PML and Sp100 (degraded proteins shown in light grey with dotted outlines). Epstein–Barr virus (EBV) BNRF1 disassembles the Daxx–ATRX histone chaperone complex, whereas HCMV pp71 degrades Daxx. Hepatitis B virus (HBV) protein HBx induces the degradation of Smc5 or Smc6. c | HSV-1 can also induce the degradation of IFI16, an alternative antiviral epigenetic repression factor, with ICP0 implicated as being involved in this degradation. d | Retroviruses avoid epigenetic repression by integrating their DNA into host euchromatin, where it can no longer be identified as foreign DNA. MLV, murine leukaemia virus.