Abstract
SEVERAL investigators have postulated that endogenous oncornaviruses play a role in development and differentiation, and that neoplasia is an unfortunate consequence of an otherwise important symbiosis1,2. Although attractive on theoretical grounds, these concepts remain unproven. Nevertheless, it is possible to study the relationship between viral gene expression and normal host functions. Evidence from several laboratories has suggested that expression of endogenous oncornavirus genes are under differentiation control in the mouse3–6. The clearest example of this is the case of gp70, the major envelope glycoprotein of the murine leukaemia viruses (MuLV)7–11. This protein which is coded for by the viral genome12 may be a component of the surfaces of cells which follow certain pathways of differentiation. Further, the thymocyte differentiation marker, GIX, has been shown to be a type-specific antigenic determinant of some gp70 molecules4,5.
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DEL VILLANO, B., LERNER, R. Relationship between the oncornavirus gene product gp70 and a major protein secretion of the mouse genital tract. Nature 259, 497–499 (1976). https://doi.org/10.1038/259497a0
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DOI: https://doi.org/10.1038/259497a0
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