Effect of cell-mediated immune factors on the replication of an attenuated temperature-sensitive mutant of vaccinia virus.
Studies of the in vivo multiplication of an attenuated temperature-sensitive strain of vaccinia virus (ts2) indicated that temperature sensitivity alone could not account for the attenuation. Immunodepressive treatment of intracerebrally inoculated mice had a dramatic stimulatory effect on the multiplication of the attenuated strain and suggested that establishment of ts2 infection in the mice was hindered by host defense mechanisms mediated by cellular elements. Experiments carried out in vitro with the 51Cr release assay showed that cells infected with the ts2 mutant represented more susceptible targets to the cytotoxic action of immune spleen cells than cells infected with the parent vaccinia strain. Moreover, it appeared that ts2 replication, compared with wild-type replication in vitro, was more inhibited by the immune spleen cells. Although this work did not evaluate the role of specifically sensitized lymphocytes within the lesions, indirect evidence suggests that lymphocytes could cause a more effective halt in ts2 virus multiplication than in wild-type multiplication.
D000818:Animals; D001921:Brain / Q000382:microbiology; D003520:Cyclophosphamide / Q000494:pharmacology; D003601:Cytotoxicity Tests, Immunologic; D003602:Cytotoxicity, Immunologic; D007111:Immunity, Cellular / Q000187:drug effects / Q000528:radiation effects; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D013696:Temperature; D014616:Vaccinia virus / Q000502:physiology*; D014779:Virus Replication; D014965:X-Rays
D003520:Cyclophosphamide