SUPPRESSION OF LYMPHOCYTE-PROLIFERATION BY PARAINFLUENZA VIRUS TYPE-3-INFECTED BOVINE ALVEOLAR MACROPHAGES

Lymphocytes stimulated with concanavalin A (Con A) or antigen in the p resence of bovine parainfluenza virus type 3 (PIV-3) infected bovine a lveolar macrophages (BAM) or monocytes, had depressed [H-3]thymidine i ncorporation. This failure of lymphocytes to incorporate radiolabel re quired live virus, was time dependent and was most pronounced when BAM were infected for 48 hr prior to the addition of lymphocytes. The rat e of infection of alveolar macrophages and the release of infectious v irus into culture supernatants paralleled suppression of lymphocyte mi togenesis by PIV-3. However, the peak titre of exogenous, live or inac tivated virus was not suppressive when added to lymphocyte macrophage cultures just prior to Con A stimulation. Neither the loss of viable a lveolar macrophages nor a shift in antigen or mitogen dose response in virally infected cultures could account for the deficit in [H-3]thymi dine incorporation by lymphocytes. Despite the presence of lymphocyte- associated virus antigen detected by direct immunofluorescence, no inc rease in PIV-3 titre above baseline was seen from infected lymphocytes , irrespective of mitogen stimulation. Likewise, lymphocytes did not c ontribute to the extracellular virus pool in lymphocyte-macrophage cul tures as the increases in viral titre above basal levels in supernatan ts were equal to levels released by macrophages alone. The expression of viral antigen on lymphocytes stimulated in the presence of PIV-3-in fected BAM suggests a non-productive or abortive infection of lymphocy tes mediated through contact with infected macrophages.