Several reports support the view that T cells play a decisive role in control of viral CNS infections. Using primary human lymphocytes, in vitro experiments demonstrated that CD8 + T lymphocytes control the dissemination of MV [39] . In resistant mouse strains the depletion of the CD4 + T cell subset by monoclonal antibodies led to a breakdown of resistance to the infection, whereas depletion of CD8 + T cells had no effect [23, 40] . In TAP-transporter deficient mice, which cannot present antigen on MHC class I molecules, MV was found to spread more transneuronally than in brains of normal mice [41] . These findings indicated that infected neurons are target cells of CD8 + lymphocytes, and that brain infections to some extent can be inhibited by CTL activity. Further investigations revealed that CD4 + T cells are able to protect either alone (in resistant mouse strains), or through cooperation with CD8 + T cells (in mice with intermediate susceptibility), and that CD8 + T cells are able to protect alone after immunization of the mice [42, 43] . Using CD46transgenic Rag-deficient mice, adoptive transfer of lymphocytes revealed that the combined activity of CD4 + T lymphocytes with CD8 + T cells or B cells is required to control the intracerebral infection [44] . Thus, most findings support the view that CD8 + T cells play an important role in the control of transneuronal virus spread, and our findings suggest that MV-specific CD8 + T cells are involved in maintaining the steady state and control of infection during the persistent phase of CNS infection.