RNA tumor viruses probably originate from the endogenous """"""""viral"""""""" information in the host cell, by accumulation of new nucleotide sequences through cycles of replication and interaction with the genomes of host cells and other viruses. Our objective is to gain detailed information of these mechanisms at the molecular level. The occurrence of changes in the genome will be studied at specific sites randomly distributed throughout the genome RNA as well as its 5' and 3' termini. In this manner, we will measure the frequency and locations of point mutations and deletion mutants that occur during the overall replication cycle of the virus as well as during replication of integrated provirus. Several spontaneous point and deletion mutants have already been isolated in such an experiment. These will be characterized both physiologically and genetically. The mechanism of recombination between viruses will be studied by examining the RNA of progeny virus from individual cells infected simultaneously with two different avian tumor viruses or with heterozygote viruses. Finally, the possibility of recombination between virus and nonviral host cell information will be examined in several different model systems.
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