Measles virus gene expression in neural cells.

Abstract

The interaction of measles virus (MV) with the human central nervous system (CNS) can lead to acute or chronic disease processes which are of clinical importance. In a fraction of patients, an acute measles encephalitis (APME) appears during or after acute measles probably as a result of virus-induced autoimmune reactions. As rare late complications of measles, subacute sclerosing panencephalitis (SSPE) and measles inclusion body encephalitis (MIBE) develop on the basis of a persistent infection in neural cells (for details see Katz, this volume). These disorders have stimulated numerous studies which have contributed to the understanding of alterations of viral gene expression and cellular gene functions in brain tissue (for review see BILLETER and CATIANEO 1991; Schneider-Schaulies and Ter Meulen 1992). Based on these investigations, it is obvious that primary interaction of MV with brain tissue is followed by a nonlytic persistent infection instituted by attenuation of viral gene functions. As convincing evidence has not been mounted for the existence of particular defective viruses initially infecting the CNS (Catianeo et al. 1989; Baczko et al. 1993), factors intrinsic or induced in neural cells have been proposed to attenuate primary viral gene expression (Kraus et al. 1992; Schneider-Schaulies et al. 1993 a,b). In this review we will give a brief overview on how defective and quantitatively altered viral gene functions encountered in persistent MV infections of brain cells may relate to cellular factors and regulatory mechanisms and how cellular gene expression in neural cells is impaired upon the interaction with MV.