Influence of toyocamycin on avian leukemia myeloblasts: cell growth, ultrastructure, RNA synthesis, and elaboration of BAI strain A virus.
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Biomedical subjects
Publications and source records attributed to J W Beard.
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Immune serum was prepared in the rabbit with BAI strain A leukosis virus isolated by centrifugal fractionation from the plasma of chickens with myeloblastic leukemia and further purified on a potassium tartrate gradient. Antibody to group-specific antigen was demonstrated in the serum by immunoelectrophoresis and immunodiffusion. Fluorescein-conjugated serum was used unabsorbed and absorbed with chick cells for study of acetone-fixed chick embryo cells uninfected or infected with strain MC29 avian leukosis virus. With unabsorbed serum, large numbers of cytoplasmic particles stained in a few cells within 2 hr after exposure to virus, and the cell number increased greatly in 24 hr. Absorption of the serum abolished the early reaction. Staining with absorbed serum was delayed until about 14 hr after culture exposure to virus, but essentially all cells were stained within 72 hr at the time when all cells were morphologically altered. Differences between the responses to unabsorbed and absorbed serum suggested cytoplasmic formation or concentration of chick tissue antigen similar to that incorporated in leukosis virus particles. The characteristics of staining with absorbed serum were similar to those observed by others in analogous studies with avian tumor viruses.
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Strain MC29 avian leukosis (myelocytomatosis) virus induced infection, elaboration of virus, and morphological alteration in chick embryo cells in vitro. Virus liberation began within 18 hr, morphological change was detectable at about 40 hr, and the cultures could be completely altered within 80 hr after infection. Altered cells were about half the volume and grew at approximately twice the rate of uninfected elements. The output of virus estimated by electron microscopy was about 140 particles per cell per hr. Deoxyribonucleic acid remained constant, but ribonucleic acid increased in both infected and control cells in adjustment to culture environment. The rates of uptake and incorporation of (3)H-uridine and the incorporation of (3)H-thymidine increased in the infected cells with onset of morphological change but were unaffected by processes of infection and virus elaboration per se. Incorporation of a (14)C-amino acid mixture was slightly greater in the infected than in control cells. The speed of continuity of infection and massive morphological alteration constitute a unique response to avian tumor viruses, and the system gives promise of singular value for detailed studies of the processes of infection and morphological change.
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