Figure 1.

Controlling the proviral/oncogenic activity during T cell activation. (A) A heterogenous population of cells can switch between different levels of activity resulting in changes of 1) the metabolic state of the cell, 2) the permissiveness of the chromatin of the provirus/oncogene that can adopt heterochromatin, euchromatin or poised chromatin structures, and 3) the availability of the transcriptional machinery, including transcription factors but also elongation, splicing and polyadenylation factors. (B) In the nucleus, the genetic locus of the provirus/oncogene in found in heterochromatin, poised chromatin (non-productive), or euchromatin (productive). Upon cell activation, the poised chromatin can allow productive transcription whereas the heterochromatin remains inactive. Transitioning between chromatin states (maroon arrows) is generally not associated with cell activation, instead it is caused by (de-) differentiation or chromatin resetting and can be induced be epigenetics drugs such as inhibitors of HDACs, BET domains, or DNMTs.