Here we investigated the role of Tregs for virus persistence in the CNS. According to our model, two week old C57BL/6 mice (an age in which these mice survive infection, while the immune system is still not fully matured) were intracerebrally infected and virus persists in a limited number of neurons in most animals for more than 10 weeks [33] . We expanded and depleted Tregs in the periphery during the persistent phase of the viral infection, and investigated whether this can be exploited to modulate the ''hidden'' CNS infection. Our data indicate that this is indeed the case and that manipulation of Tregs can be utilized to regulate virus-specific CD8 + effector T cells and virus persistence in the brain.