Persistent measles virus infection of murine neuroblastoma cells differentially affects the expression of PKC individual isoenzymes.

Measles virus (MV) is among the infectious agents displaying a propensity for establishing persistent infections of the CNS. It is assumed that continuous presence of MV defective particles or viral genome in persistently infected cells may influence host cellular processes and perturb biochemical signal transduction pathways operating in linkage to various cell surface receptors. PKC expression in a MV persistently infected neuroblastoma cell line (NS20Y/MS) was investigated. The relative levels of PKC isoenzymes were determined by Western blot analysis. We found that protein levels of PKCalpha, epsilon and zeta, but not PKCdelta, were increased in NS20Y/MS cells. PKCbeta, gamma and eta were undetectable. Treatment of NS20Y/MS cells with anti-MV Abs, which downregulated MV protein synthesis, also reduced PKCalpha expression to the basal level observed in the uninfected NS20Y cells. Our results suggest that a persistent MV infection has specific effects on the expression of certain PKC isoenzymes. We postulate that the MV-associated neurologic changes may reflect virus induced changes in biochemical signaling pathways and that these effects are likely to be regulated by the host's anti-viral humoral immune response.