Letter | Published:

Activation of non-expressed bovine papilloma virus genomes by tumour promoters

Nature volume 296, pages 675677 (15 April 1982) | Download Citation

Subjects

Abstract

Naturally occurring cancer seems to be a multiple-hit phenomenon resulting from the interaction of several factors. Numerous environmental carcinogens on one hand and the widespread tumour viruses on the other, are capable of either transforming cells in vitro or inducing tumours in vivo. A few years ago, based on epidemiological evidence, a possible interaction between bovine papilloma viruses and an environmental carcinogen in bracken fern was noted in conjunction with alimentary cancer in cattle1. We report here that tumour-promoting agents which by themselves are unable to transform cells, are capable of inducing the transcription of bovine papilloma virus type 1 (BPV-1) in mouse embryo fibroblast (MEF) tissue cultures, where the viral genomes reside in a non-expressed episomal state after infection. In such cells, one brief treatment with the tumour promoter results in the transcription of the same viral mRNA species present in BPV-1-induced tumours and in BPV-1-transformed cells. Furthermore, viral DNA is replicated and the cells acquire the transformed phenotype. Once activated, these properties remain stable. This interaction between tumour promoters and latent inactive tumour virus genomes leads, in appropriate cell systems, to the activation of particular viral genes and to the transformed phenotype of the host cells.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1.

    , , , & Nature 274, 215–217 (1978).

  2. 2.

    et al. C. r. hebd. Séanc. Acad. Sci., Paris 257, 2328–2331 (1963).

  3. 3.

    , , & Arch envir. Hlth 19, 827–837 (1969).

  4. 4.

    , & Proc. natn. Acad. Sci. U.S.A. 74, 524–528 (1977).

  5. 5.

    , , & Nature 199, 1016–1018 (1963).

  6. 6.

    , , , & Nature 201, 423–424 (1964).

  7. 7.

    , & J. Virol. 35, 962–964 (1980).

  8. 8.

    , , , & Proc. natn. Acad. Sci. U.S.A. 78, 2727–2731 (1981).

  9. 9.

    Virology 108, 251–255 (1981).

  10. 10.

    , & Virology 115, 414–418 (1981).

  11. 11.

    , , & J. Virol. 39, 945–949 (1981).

  12. 12.

    , , & Nature 293, 749–751 (1981).

  13. 13.

    , & Proc. natn. Acad. Sci. U.S.A. 68, 1876–1880 (1971).

  14. 14.

    & J. Virol. (in the press).

  15. 15.

    J. Virol. 43, 473–487 (1979).

  16. 16.

    J. molec. Biol. 98, 503–517 (1975).

  17. 17.

    , , & Nature 272, 373–375 (1978).

  18. 18.

    , & FEBS Lett. 128, 191–194 (1981).

  19. 19.

    Proc. natn. Acad. Sci. U.S.A. 77, 5201–5205 (1980).

  20. 20.

    , , & Proc. natn. Acad. Sci. U.S.A. 78, 7722–7726 (1981).

  21. 21.

    , & Infect. Immunity 31, 1214–1222 (1981).

  22. 22.

    et al. Proc. natn. Acad. Sci. U.S.A. 78, 6446–6450 (1981).

Download references

Author information

Affiliations

  1. Institute for Virus Research, German Cancer Research Center, 6900 Heidelberg, FRG

    • Eberhard Amtmann
    •  & Gerhard Sauer

Authors

  1. Search for Eberhard Amtmann in:

  2. Search for Gerhard Sauer in:

About this article

Publication history

Received

Accepted

Published

DOI

https://doi.org/10.1038/296675a0

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.