Fig 1.

Tr and E reduce HSV-2 replication in genital ECs, and E has greater anti-HSV-2 activity than Tr. Genital ECs were left untreated (UT) or treated with an MOI of 0 to 50 of Ad/dl or Ad/Tr and inoculated with HSV-2 at an MOI of 0.1 to 5. Viral titers in supernatants were determined 24 h postinfection by standard plaque assay and presented as log-transformed PFU/ml for HEC-1A cells (A) and for End1/E6E7 (B). In panels C and D, HEC-1A cells were pretreated with Tr (C) and E (D) for 1 h and subsequently exposed to HSV-2 at an MOI of 1 for 2 h and, after repeated washes, cultured for an additional 24 h. Viral titers were determined in supernatants by plaque assay. For all, the data are shown as the means ± SD and are representative of three independent experiments performed in triplicate. Statistical analysis was performed using Student's t test (A, B) or ANOVA with Tukey's post hoc test (C, D), with significance indicated in graphs. For determining IC₅₀s of Tr and E anti-HSV-2 activity, readouts from dose-dependent functional studies were used for determining efficiency parameters of relevant experimental points. The maximum inhibitory effect was considered 100% effect, and the other values were computed accordingly and plotted against relevant doses of Tr (*) and E (●) as percentages of maximal inhibitory effect. (E) The relevant IC₅₀s for Tr and E are indicated with a filled arrowhead and an open arrowhead, respectively, pertaining to inhibitory effects of Tr and E on HSV-2 infectivity of HEC-1A cells. Error bars, SD.