For the depletion of Tregs we used transgenic mice expressing the human diphtheria toxin (DT) receptor under the control of the Foxp3-promoter, which can be treated with DT to eliminate specifically Foxp3 + Tregs (DEREG-mice) [38] . To test the activity of the DT-batch used, adult DEREG mice were in a pilot experiment treated with DT under standard conditions (1 mg DT i.p. injected at 6 consecutive days) and analyzed the next day. Lymphocytes isolated from the spleen and lymph nodes were analyzed by flow cytometry to demonstrate the successful depletion of Foxp3 + GFP + Tregs by more than 90% (Fig. 4 A) . In order to assess the effect of Treg depletion on virus persistence in young mice, persistently infected mice were treated at 3 consecutive days (at day 17, 18, and 20 post infection) with 1 mg DT and analyzed at day 28 post infection ( Fig. 4 B) . In these mice, the viral infection was again quantified histologically in subsequent brain slices through the complete cerebrum as described earlier [33] . Treg depletion in DEREG 2/+ mice (compared to DT- treated DEREG 2/2 mice as control animals) led to a significant reduction of the number of infected neurons from brains of persistently infected animals (n = 6, P = 0.0098; Fig. 4 C) .