Sendai virus irradiated by UV light, the dose of which is sufficient for inactivation of infectivity, is capable of inducing synthesis of early protein only. The synthesis of early virus-specific proteins was observed in the absence of virusspecific RNA-synthesis. Consequently, RNA of virion (plus-strand) is the m-RNA for the synthesis of early virus-specific proteins of Sendal virus. Since viral structural proteins do not synthesize under these conditions, it is assumed, that the synthesis of virus capsid proteins is coded by a minus-strand. The possible significance of such processes for an understanding of the nature of viral oncogenesis and stable antiviral immunity is discussed. 21"
Transformation of embryonic human fibroblasts was obtained by treatment with inactivated Sendai virus and polyoma virus. Transformed cells differed morphologically from normal cells and formed a stable cell line ( P -2The discovery that Rous sarcoma virus can produce tumours in mammals considerably changed previously held ideas about the limited specificities of tumour viruses. At the same time the notion of the spectrum of pathogenicity of tumour viruses remained unchanged. Polyoma virus induces tumours in rodents and transforms their cells in vitro, but does not affect human or chicken cells. If this cellular resistance could be overcome it would be possible to study new cell-virus relationships and also the role of cocancerogens in the aetiology of human and animal tumours. These new co-cancerogenic factors may be operative as helper factors not only in virus cancerogenesis but also in the tumour development induced with chemical cancerogens.In our experiments we transformed embryonic human skin-muscle tissues with polyoma virus, human adenovirus of type 12 and Rous sarcoma virus. Peculiar virus transformation of human tissues took place after treatment of the cells by these viruses and inactivated Sendai virus.
MATERIAL AND METHODSWe used the myxovirus parainfluenza group I, strain Sendai, which had been cultured in allantoic cells of 9-day-old chicken embryos. Infections were initiated in these embryos with 0.1 ml of Infected allantoic fluid was inactivated with B-propiolactone in a final concentration of 0.1 % to dilution of Sendai virus.
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