Viral infections of the brain mostly represent clinically important, often life-threatening complications of systemic viral infections. For example, after acute measles, CNS complications may occur early as acute post-infectious encephalitis, or after years of viral persistence as subacute sclerosing panencephalitis (SSPE). Epidemiological studies indicated that the primary MV infection of SSPE patients takes place predominantly below the age of two years, when the immune system of the host is still immature and residual maternal antibodies may be absent or not sufficient for complete virus neutralization [20, 21] . For intracerebral MV infection of mice, a transgenic human receptor for MV is not necessarily required, and various infection models exist depending on the age of the mice, the virus strain, and the infectious dose [22, 23, 24, 25, 26] . As found in genetically unmodified and MVreceptor transgenic mice, T cells and IFN-c have a critical role for protection and clearance of virus from the brain [27, 28, 29, 30] . Transient immunosuppression during MV-infection enhanced virus replication and facilitated persistence [31] . After intranasal infection of MV-receptor CD150-transgenic mice, a specific antiviral cellular immune response including an increased proportion of Foxp3 + Tregs in the spleen was observed [32] . Although the presence and activity of Tregs has been demonstrated, their actual role in viral immunosuppression or immunopathogenesis in the brain remains to be elucidated.