Measles Virus can give three different forms of infections in the cent
ral nervous system. These are acute postinfectious encephalitis, acute
progressive infectious encephalitis, and subacute sclerosing panencep
halitis (SSPE). The postinfectious acute disease is interpreted to ref
lect an autoimmune reaction. The acute progressive form of brain disea
se, also referred to as inclusion body encephalitis, reflects a direct
attack by the virus under conditions of yielding cell-mediated immuni
ty. The late progressive form of encephalitis (SSPE) has been extensiv
ely analyzed. Recent molecular genetic studies have unravelled a range
of mechanisms by which a defective expression of either the matrix, t
he 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 a
nd animal origin. Some of the findings are reviewed. Experimental anim
als, in particular rodents, have been used to establish systems in whi
ch 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 discusse
d. More recently, mice with genetic defects in immune functions were u
sed to evaluate consequences as to initiation and dissemination of vir
us infection in the brain. (C) 1997 Elsevier Science Inc.