Skip to main content
. 2016 May 27;35(13):1385–1399. doi: 10.15252/embj.201593458

Figure 6. ICP27 from the simplex virus genera of alpha‐herpesviruses inhibits IFN production in a manner dependent on the RGG box.

Figure 6

  • A, B
    Alignment of the ICP27 homologs of the human herpesviruses (A) and a series of alpha‐herpesviruses (B). The diagram to the right illustrates the degree of similarity with HSV‐1 ICP27 and the distribution within the molecules.
  • C
    THP1 cells were infected with HSV‐1 (KOS), HSV‐2 (HG52), HSV‐1 ΔICP27, or HSV‐1 ΔICP27 rescued with HSV‐2 ICP27 (MOI 3). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
  • D
    RAW264.7 cells were infected with HSV‐1 (KOS), PRV (vBecker3) and the corresponding mutants lacking ICP27 (UL54 in the case of PRV). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
  • E
    Alignment of the RGG box of in ICP27 proteins of the simplex virus genera of alpha‐herpesviruses.
  • F
    THP1 cells were infected with HSV‐1 (KOS), ΔRGG, or ΔICP27 (MOI 3). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity. ICP27 expression in the infected cells was determined by Western blotting.
  • G
    THP1 cells were infected with HSV‐1 KOS or HSV‐1 ΔRGG (MOI 10) for 8 h, and total lysates were generated. STING was immunoprecipitated and subjected to Western blotting using antibodies against ICP27 and STING.
Data information: Data in (C, D, and F) are presented as means of triplicates ± SD; symbols for P‐values: *0.01 < P < 0.05; **0.001 < P < 0.01; ns, not significant.Source data are available online for this figure.