Infection of mouse preimplantation embryos with simian virus 40 and polyoma virus

Publisher Website
Google Scholar
Abstract
Mouse 2-cell embryos, morulae and blastocysts were killed when infected in vitro with SV-40 at high multiplicities of infection. Polyoma virus was not deleterious for preimplantation embryos, even at a very high multiplicity of infection, but the outgrowths of polyoma-infected blastocysts disintegrated after several days of culture. Indirect immunofluorescence tests revealed the presence of SV-40 T [tumor] and V [capsid] antigens and polyoma virus V antigen in the nuclei of trophoblastic cells. Virus-specific antigens were not found in the nuclei of cells forming inner cell masses of blastocysts or in inner cell mass-derived cells in blastocyst outgrowths. The appearance of SV-40 T and V antigens in the nuclei was inhibited by .alpha.-amanitine, a RNA polymerase II inhibitor. The amount of infectious virus recovered from cultures of morulae or blastocysts on subsequent days after infection with SV-40 initially declined but later increased. Some cells of early mouse embryos are apparently permissive for the expression of early and late functions of SV-40 genome and susceptibility to infection with polyoma virus and/or permissiveness for the expression of polyoma virus late functions develop gradually between the 2-cell and blastocyst stages. EM observations showed the presence of specific complexes of membranes and virions in the cytoplasm of trophoblastic cells. Single viral particles could be found in the nuclei and also in mitochondria.