Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • NEWS AND VIEWS

Epstein–Barr virus is an agent of genomic instability

A protein from Epstein–Barr virus called EBNA1 has been shown to bind to and break human chromosome 11, producing instability in the genome that might cause a predisposition to cancer.
  1. Lori Frappier

    1. Lori Frappier is in the Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1M1, Canada.

    View author publications

    You can also search for this author in PubMed  Google Scholar

Epstein–Barr virus (EBV) is a common herpesvirus that is also associated with several types of cancer, including lymphomas, nasopharyngeal carcinomas and gastric carcinomas1. How exactly the virus affects the development of these cancers is unclear, but tumour cells are known to be derived from infected cells that express a small subset of EBV proteins. In fact, the only viral protein that is expressed in all types of EBV-related cancer is Epstein–Barr nuclear antigen 1 (EBNA1), which binds to specific sequences in the viral DNA, allowing it to persist and replicate. The possibility that this protein contributes directly to cancer has long been proposed and disputed2. Writing in Nature, Li et al.3 suggest how it might do so — by binding to a specific region on human chromosome 11 and triggering its breakage, thereby inducing genomic instability.

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Learn more

Prices may be subject to local taxes which are calculated during checkout

Nature 616, 441-442 (2023)

doi: https://doi.org/10.1038/d41586-023-00936-y

References

  1. Farrell, P. J. Annu. Rev. Pathol. 14, 29–53 (2019).

    Article  PubMed  Google Scholar 

  2. Frappier, L. Viruses 4, 1537–1547 (2012).

    Article  PubMed  Google Scholar 

  3. Li, J. S. Z. et al. Nature 616, 504–509 (2023).

    Article  Google Scholar 

  4. Ambinder, R. F., Shah, W. A., Rawlins, D. R., Hayward, G. S. & Hayward, S. D. J. Virol. 64, 2369–2379 (1990).

    Article  PubMed  Google Scholar 

  5. Rawlins, D. R., Milman, G., Hayward, S. D. & Hayward, G. S. Cell 42, 859–868 (1985).

    Article  PubMed  Google Scholar 

  6. Bochkarev, A. et al. Cell 84, 791–800 (1996).

    Article  PubMed  Google Scholar 

  7. Frappier, L. Curr. Top. Microbiol. Immunol. 391, 3–34 (2015).

    PubMed  Google Scholar 

  8. Lu, F. et al. Virol. J. 7, 262 (2010).

    Article  PubMed  Google Scholar 

  9. Saridakis, V. et al. Mol. Cell 18, 25–36 (2005).

    Article  PubMed  Google Scholar 

  10. Sarkari, F. et al. PLoS Pathol. 5, e1000624 (2009).

    Article  Google Scholar 

  11. Sivachandran, N., Wang, X. & Frappier, L. J. Virol. 86, 6146–6158 (2012).

    Article  PubMed  Google Scholar 

  12. Frappier, L. & O’Donnell, M. Proc. Natl Acad. Sci. USA 88, 10875–10879 (1991).

    Article  PubMed  Google Scholar 

  13. Avolio-Hunter, T. M., Lewis, P. N. & Frappier, L. Nucleic Acids Res. 29, 3520–3528 (2001).

    Article  PubMed  Google Scholar 

Download references

Competing Interests

The author declares no competing interests.

Subjects

Latest on:

Nature Careers

Jobs

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing

Search

Advanced search

Quick links