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Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model
Published on: October 16, 2017
Phenotypic mixing in the avian tumor virus group
1Department of Pathology, University of Colorado Medical School, Denver, Colorado 80220, USA.
Abstract:
Mixed infection of chick embryo fibroblasts with avian tumor viruses of subgroups A and B yields progeny virus in which properties of both parental subgroups are combined. Such combination forms of avian tumor virus have an expanded host range on genetically resistant chicken cells. This allows virus particles with a subgroup A genome to enter into C A cells from which subgroup A virus is otherwise excluded. Likewise, mixedly grown virus particles with a subgroup B genome can be shown to replicate in C B cells which are insusceptible to pure subgroup B stocks. The ability of combination forms to overcome host range barriers appears to result from the presence of subgroup A and B envelope antigens in individual virus particles. Neutralization experiments with antibody also indicate that the envelope of many mixedly grown avian tumor virus particles contains a mosaic of A and B antigens. Chicken serum specific against subgroup A envelope antigen prevents subgroup B genomes in mixedly grown virus from entering C B cells. Conversely, anti B serum neutralizes infectivity of subgroup A genomes on C A cells. The combination of subgroup A and B characteristics in particles of mixedly grown avian tumor virus preparations is genetically unstable at low multiplicities of infection. Most of the combination forms appear to be caused by phenotypic mixing but the occurrence of heterozygotes or of a small percentage of recombinants cannot be excluded.
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