FIG 5.

KOS(M) genomes are maintained at higher copies overall during latency and reactivation than with 17syn⁺ but are not significantly replicated following PI3K inhibitor-induced reactivation. (A) HSV-1 strain KOS(M) maintains significantly higher genome copies than 17syn⁺ during latency as well as during PI3K inhibitor-induced reactivation in LUHMES. Reactivation was induced at day 8 postinfection (0 h) with 10 μM Ly294002, and cultures were harvested for qPCR at the indicated times using primers and probes against UL30. (B) 17syn⁺ genome copies have been significantly replicated by 12 h postreactivation (compared to 0 h). (C) HSV-1 strain KOS(M) genome copies were determined as described above. We found no significant difference in genomes copy number during reactivation compared to that at 0 h, implying fewer genomes were replicated. For each time point, significance was determined by ordinary two-way ANOVA with Sidak’s multiple-comparison test across 6 biological replicates (*, P < 0.05; ***, P < 0.0001) (n = 6).