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

Figure 1. HSV‐1 harbors a mechanism to inhibit type I IFN expression, which is dependent on viral gene expression but independent of ICP0.

Figure 1

  1. THP1 cells were infected with the shown strains of HSV‐1 (MOI 3). Supernatants were harvested from untreated cultures or cells infected for 12 or 18 h for measurement of type I IFN bioactivity.
  2. THP1 cells were treated with 0.1 μg/ml of acyclovir (ACV) and infected with the KOS and F HSV‐1 strains (MOI 3). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
  3. THP1 cells were treated with infectious or UV‐inactivated HSV‐1 (strain KOS). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
  4. MDMs were infected with ICP0‐deficient or revertant HSV‐1 (strain KOS, MOI 3). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
  5. THP1‐derived cells deficient for cGAS or STING were infected with the shown strains of HSV‐1 (MOI 3) or stimulated with poly(I:C) (2 μg/ml). Supernatants were harvested 18 hpi for measurement of type I IFN bioactivity.
Data information: Data are presented as means of triplicates ± SD; symbols for P‐values: **0.001 < P < 0.01; ***P < 0.001; ns, not significant.