Immunosuppression by measles virus strains: Relationship to virus replication

143 INACTIVATED MEASLES VIRUS ANTIGEN.

VIRUS

SUPPRESSES

THE IMMUNE RESPONSE

TO HERPES

SIMPLEX

R.H. SMITH, M.J. M#KEL# and A.A. SALMI, Viral Pathogenesis Research Unit, Department of Medical Microbiology and Infectious Diseases, University of Alberta, Bdmonton, Alberta, Canada T6G ZHI. Measles virus (MV) infection causes a transitory immunosuppression. More including a direct effect of MV replication in than one mechanism, immunological cells, is reponsible for such suppression. We have shown that purified, 8-propiolactone inactivated MV can suppress the murine T-cell immune response to inactivated herpes simplex virus (HSV) antigen both in viva and in vitro. If MV was added at the time of HSV immunization of Balb/C response was suppressed as compared to mice, the in vitro HSV blastogenic However, if were HSV proliferative mice the normal response. cyclophosphamide (CP) pre-treated 2 days before HSV-MV immunization, the HSV As CP has been show to have a prefrential response was not suppressed. effect on suppressor T cells, the results suggest an involvement of suppressor T-cells in the MV-innnunosuppression. We have further demonstrated that inactivated, purified MV suppresses the blastogenic response of human peripheral blood lymphocytes to inactivated herpes simplex virus (HSV) antigen showed that MV significantly in vitro. A time course experiment suppresses the HSV blastogenic response when added to the cultures up to 48 hours after stimulation with HSV. Both the in vivo and in vitro Mv induced and not due to immunosuppression was virus-specific, cross-reactive cellular components, as neither purified inactivated vesicular stomatitis virus, mumps virus nor VERO cell lysate antigen could suppress the HSV cellular immune response. These results indicate that MV proteins have irmnunosuppressive properties.

144 IMMUNOSUPPRESSION REPLICATION.

BY

MEASLES

VIRUS

STRAINS:

RELATIONSHIP

S. VYDELINGUM, K. SURYANARAYANA, R.G. MARUSYK, A.A. SALMI, Viral Pathogenesis Research Unit, Medical Microbiology and Infectious Diseases, Alberta, Edmonton, Alberta, Canada T6G 2H7

TO

VIRUS

and Department University

of of

Measles virus (MV) infection inhibits lymphocyte functions both in vitro and in viva. In an attempt to understand the events occurring during MVimmunosuppression, we have characterized the interaction of different MV strains, including a temperature sensitive mutant (MVts38), with peripheral blood mononuclear cells. The extent of isununosuppression by different virus strains varied considerably. The MVts38 inhibited lymphocyte mitogenesis both at the non-restricted (32OC) and restricted (37OC and 39OC) temperatures. Although no infectious virus was released at the restricted immunofluorescence data indicated that all the major temperatures, structural polypeptides were expressed. To compare RNA replication and transcription in lymphocytes with different degrees of MV-induced immunosuppression, we have used strand-specific gene probes in northern blot hybridization experiments. The cDNA inserts of MV genes were cloned into Ml3 vectors and the resulting templates were used as probes. The sub-genomic transcripts of PHA-stimulated PBL infected with different strains MV were comparable in size to those reported for MV-infection in permissive laboratory cell lines. Bicistronic readthrough transcripts were observed with N, P/C and M genes. The results indicate that a full cycle of virus replication is not necessary for inrmunosuppression by MV.

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