Subject(s)
Antigens, Viral , Immunization , Lymphoma/immunology , Newcastle disease virus/immunology , Peritoneal Neoplasms/immunology , Respirovirus/immunology , AKR murine leukemia virus , Animals , Antigens, Neoplasm , Cell Fractionation , Cell Membrane/immunology , Female , Freund's Adjuvant/pharmacology , Graft Rejection , Lymphoma/microbiology , Male , Mice , Mice, Inbred C3H , Mycobacterium bovis/immunology , Neoplasm Transplantation , Peritoneal Neoplasms/microbiology , Transplantation, Homologous , Ultracentrifugation , Virus ReplicationABSTRACT
Antiviral antibody and rabbit complement added as early as 5 min after infection, and with relatively low virus/cell multiplicity, lysed mouse ascites lymphoma cells infected with Sendai or Newcastle disease virus. Inactive Sendai virus at much higher input also sensitized ascites cells and mouse fibroblast monolayers to early antiviral immune cytolysis. At 4 C where adsorption but no penetration occurred, antibody removed virus from the cell membrane and little cytolysis was observed. The ascites cells were sensitive to antibody and complement at all times after the start of penetration and uncoating, indicating that viral envelope antigen is constantly present on the cell membrane. Significant cross-reactions by immune cytolysis between Newcastle disease virus- and Sendai virus-infected cells suggested possible participation of host antigens of the viral envelope. No comparable antiviral immune cytolysis was observed with influenza strains PR8 and WSN. Cell viability was estimated by dye exclusion and the ability to form acid from glucose as indicated by colorimetric pH of the medium. The relation of antiviral immune cytolysis to changes in the membrane resulting in cell fusion is considered.
