Measles virus in the CNS: the role of viral and host factors for the establishment and maintenance of a persistent infection.

Acute measles (for review see: Grif®n and Bellini, 1996) can be accompanied by early or late central nervous system (CNS) complications. These include the acute postinfectious measles encephalitis (APME), which develops 2 ± 4 weeks after infection, or as late complications, the measles inclusion body encephalitis (MIBE) in immunocompromised patients, and the subacute sclerosing panencephalitis (SSPE) months to years after the initial infection (Table 1). With an incidence of approximately 0.1%, APME is the most frequent, however also the least well understood disease measles associated neurological complication. Since myelin basic protein-speci®c T cells can be isolated from patients, APME is thought to have an autoimmune etiology (Johnson et al, 1984). The two late complications, MIBE and SSPE, are based on persistent measles virus (MV) infections in the brain. In this review we will give a brief overview on a number of virological and immunological ®ndings obtained from MV infected patients, from animal models with MV-induced encephalitis (MVE), and from MV infected primary and permanent neural tissue cultures (for review see Schneider-Schaulies et al, 1997).