Measles virus can give three different forms of infections in the central nervous system. These are acute postinfectious encephalitis, acute progressive infectious encephalitis, and subacute sclerosing panencephalitis (SSPE). The postinfectious acute disease is interpreted to reflect an autoimmune reaction. The acute progressive form of brain disease, also referred to as inclusion body encephalitis, reflects a direct attack by the virus under conditions of yielding cellmediated immunity. The late progressive form of encephalitis (SSPE) has been extensively analyzed. Recent molecular genetic studies have unravelled a range of mechanisms by which a defective expression of either the matrix, the fusion, or the hemagglutinin proteins may lead to viral persistence in brain cells under conditions not allowing identification by immune surveillance mechanisms. Many aspects of virus-cell interactions have been examined by use of explant cultures of neuronal cells of human and animal origin. Some of the findings are reviewed. Experimental animals, in particular rodents, have been used to establish systems in which phenomena, pivotal to the evolution of acute as well as persistent measles virus infections in the brain, can be studied. A wide range of potentially important mechanisms has been highlighted and is discussed. More recently, mice with genetic defects in immune functions were used to evaluate consequences as to initiation and dissemination of virus infection in the brain.