Pathogenic aspects of measles virus infections

Measles virus (MV) infections normally cause an acute self limiting disease which is resumed by a virus-specific immune response and leads to the esta blishment of a lifelong immunity. Complications associated with acute measl es can, on rare occasions, involve the central nervous system (CNS). These are postinfectious measles encephalitis which develops soon after infection , and, months to years after the acute disease, measles inclusion body ence phalitis (MIBE) and subacute sclerosing panencephalitis (SSPE) which are ba sed on a persistent MV infection of brain cells. Before the advent of HIV, SSPE was the best studied slow viral infection of the CNS, and particular r estrictions of MV gene expression as well as MV interactions with neural ce lls have revealed important insights into the pathogenesis of persistent vi ral CNS infections. MV CNS complication do, however, not large contribute t o the high rate of mortality seen in association with acute measles worldwi de. The latter is due to a virus-induced suppression of immune functions wh ich favors the establishment of opportunistic infections. Mechanisms underl ying MV-mediated immunosuppression are not well understood. Recent studies have indicated that MV-induced disruption of immune functions may be multif actorial including the interference with cytokine synthesis, the induction of soluble inhibitory factors or apoptosis and negative signalling to T cel ls by the viral glycoproteins expressed on the surface of infected cells, p articularly dendritic cells.