The de-repression of latent infections observed in J-LatA2 and J-Lat 11.1 cells in response to depletion of the BAF complex subunits BAF250, INI-1, and BRG1 indicated that the BAF complex is necessary to maintain silencing at the LTR during a latent infection (Fig 3). Here, SMARCB1 is linked to disease arising from reactivation of latent virus.