Skip to main content
. 2014 May;88(10):5421–5436. doi: 10.1128/JVI.03763-13

FIG 7.

FIG 7

Role of TLR9 signaling in the induction of chemokine secretion by HHV-6A. (A) Primary cultures of CD46-transgenic mice were inoculated with either UV-inactivated or infectious HHV-6A or mock solution. Control stimulations with LPS and CpG were performed in parallel. During stimulation, cells were treated with the TLR9 antagonist ligand ODN 2088 (black bars) or left untreated (gray bars). CCL5, CXCL10, and CCL2 mRNA expression was analyzed 24 h after stimulation. Means and standard deviations from 4 independent experiments are presented. (B) HEK cells stably expressing human TLR9 and the luciferase reporter construct were stimulated with UV-inactivated or infectious HHV-6A and HHV-6B at an MOI of 0.5, 1, or 2 in triplicate. Nonstimulated (DMEM), mock-stimulated, and CpG-stimulated controls were analyzed in parallel. Means and standard errors of the means from three independent experiments are presented. (C) hTLR9-HEK reporter cells were treated with the TLR9 antagonist ODN 2088 or left untreated and then were stimulated with HHV-6A. Luminescence values are expressed relative to the nonstimulated DMEM control. Means and standard deviations of triplicate values from one representative of three independent experiments are plotted (*, P ≤ 0.05; Mann-Whitney test).

HHS Vulnerability Disclosure