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Reversal of the measles virus-mediated increase of phosphorylating activity in persistently infected mouse neuroblastoma cells by anti-measles virus antibodies

M. Wolfson^1,

¹ Ben Gurion University of the Negev, Department of Microbiology and Immunology, P.O. Box 653, 84105 Beer Sheva, Israel
² Institut für Virologie und Immunbiologie, Universität Würzburg, Versbacher Strasse 7, 97078 Würzburg, Germany
and³ New Jersey Medical School-UMDNJ, Department of Medicine, Newark, New Jersey 07163, U.S.A.

To investigate the effect of persistent measles virus infection on signal transduction in cells of neuronal origin, the mouse neuroblastoma cell line NS20Y/MS, which is persistently infected with measles virus, was used. The results demonstrate an approximate 50% increase in total phosphorylation and a similar increase in protein kinase C (PKC) activity. Western blot analysis with anti-total PKC or anti-PKC- antibodies revealed a significant increase in the level of an 80K immunoreactive PKC in NS20Y/MS cells. Following incubation of NS20Y/MS cells with polyclonal anti-measles virus antibodies, which down-regulate the level of measles virus proteins, total and PKC-mediated phosphorylation returned to the basal level of uninfected cells. This effect was reversible and removal of the antibodies resulted in restoration of the high level of total and PKC-mediated phosphorylation. The release of infectious measles virus was strongly inhibited by incubation of NS20Y/MS cells with the PKC inhibitor, 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7). These results demonstrate that measles virus induces elevation in cellular phosphorylation which is essential for measles virus production.

Present address: Department of Molecular Pharmacology, Albert Einstein School of Medicine of Yeshiva University, 1300 Morris Park Avenue, Bronx, New York, New York 10461, U.S.A.

Received 1 September 1993; accepted 12 November 1993.