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. 2020 Dec 22;9:e58037. doi: 10.7554/eLife.58037

Figure 1. HSV-1 Reactivation from sympathetic neurons is induced by adenylate cyclase activation.

Figure 1.

(A) Schematic of the primary sympathetic superior cervical ganglia (SCG)-derived model of HSV latency. Reactivation was quantified based on Us11-GFP-positive neurons in presence of WAY-150168, which prevents cell-to-cell spread. (B) Schematic of the cellular pathways activated by forskolin treatment. Forskolin can act both intracellularly to activate adenylate cyclase (AC) and increasing the levels of cAMP or extracellularly on ion channels. (C) Numbers of Us11-GFP-positive neurons following addition of either forskolin (60 μM) or cell-impermeable dideoxy-forskolin (60 μM) treatment of latently-infected sympathetic neurons. (D) Numbers of Us11-GFP-positive neurons following treatment with a cAMP mimetic 8-Bromo-cAMP (125 μM). (E) Reactivation, quantified by Us11-GFP-positive neurons, was induced by forskolin in the presence or absence of the adenylate cyclase inhibitor SQ22,536 (50 μM). In C-E each point represents a single biological replicate, and the mean and standard errors of the mean (SEM) are also shown. In D statistical comparisons were made using an unpaired t-test. In C and E statistical comparisons were made using a one-way ANOVA with a Tukey's multiple comparisons test. *p<0.05, **p<0.01.

Figure 1—source data 1. Quantification of GFP-positive neurons for Figure 1.