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. 2018 Jan 8;14(1):e1006769. doi: 10.1371/journal.ppat.1006769

Fig 8. Dual roles for PML and IFI16 in the regulation of intrinsic and innate immunity to HSV-1 infection.

Fig 8

(A) HFt cells were DMSO or Ruxolitinib (5μM; Ruxo) treated and infected with serial dilutions of WT or ΔICP0 HSV-1 for 24 h prior to immuno-staining for plaque formation. Plaque counts expressed relative to control cell monolayers (# of plaques treated / # of plaques DMSO control) at equivalent serial dilutions of virus and presented as relative plaque formation efficiency (PFE). n ≥ 3, means and standard deviations shown. (B) HFt cells were DMSO or Ruxo treated and infected with WT (MOI 0.001 PFU/cell) or ΔICP0 (MOI 1 PFU/cell) HSV-1. Cell released virus (CRV) was harvested at the indicated times (hpi) and CRV titres determined on U2OS cells. n = 3, means and standard deviations shown. (C) Stably transduced HFt cells expressing non-targeting control (shCtrl), or targeting IFI16 (shIFI16) or PML (shPML) shRNAs, were infected with WT or ΔICP0 HSV-1 (as in A). Plaque counts expressed relative to infected shCtrl cell monolayer plaque counts (1) and presented as relative PFE. n = 3, means and standard deviations shown. (D) shCtrl, shIFI16, or shPML HFt cells were treated with DMSO or Ruxo and infected with either WT or ΔICP0 HSV-1 (as in B). CRV was collected at the indicated times (hpi) and titres determined on U2OS cells. n = 3, means and standard deviations shown. (E, F) Relative Mx1, ISG15, and ISG54 mRNA levels in HFt shCtrl, shIFI16, or shPML cells mock or ΔICP0 infected (MOI 1 PFU/cell) at 9 hpi. n = 3, means (RQ) and standard deviations (RQmin/max) shown and expressed relative to ΔICP0 infected shCtrl (1). *** P < 0.001; two-tailed t-test.