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. 2020 Jan 22;9:e52168. doi: 10.7554/eLife.52168

Figure 7. Inhibition of interferon signaling increases viral gene expression and promotes reactivation.

(A and B) HCMV- infected monocytes were treated at 3hpi with interferon signaling inhibitor, ruxolitinib (ruxo), or left untreated, and analyzed for gene expression level, by RNA-seq. (A) Expression of interferon-induced genes at 3dpi (left) and 6dpi (right). (B) Expression of viral genes at 3dpi (left) and 6dpi (right). (C) Viral gene expression in HCMV- infected monocytes that were treated with ruxo at 1, 2, 3dpi or left untreated was measured by RNA-seq at 5dpi. P values for (A-C), calculated using likelihood ratio test on logistic regression of viral reads, are indicated. (D) HCMV- infected monocytes were treated at 3hpi with interferon signaling inhibitor, ruxolitinib (ruxo), or left untreated, and at 6dpi, equivalent numbers of monocytes were co-cultured with fibroblasts to induce reactivation. Viral reactivation in ruxo treated vs. untreated cells was assessed by count of GFP positive plaques formed on the fibroblasts. Means and error bars (reflecting standard deviation) were calculated from 2 independent biological repeats. P value as calculated using likelihood ratio test on Poisson regression of positive plaque events is indicated.

Figure 7.

Figure 7—figure supplement 1. Uniform induction of expression across viral genes by inhibition of interferon signaling.

Figure 7—figure supplement 1.

Scatterplot showing read number of all viral genes in ruxolitinib treated cells compared to untreated cells at (A) 3dpi and (B) 6dpi.