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.

  • Matters Arising
  • Published:

Beta human papillomaviruses and skin cancer

Nature volume 588, pages E20–E21 (2020)Cite this article

Subjects

Matters Arising to this article was published on 16 December 2020

The Original Article was published on 30 October 2019

arising from J. D. Strickley et al. Nature https://doi.org/10.1038/s41586-019-1719-9 (2019)

Much of the data in the Strickley et al. paper was obtained in studies of laboratory mice that, upon infection with a mouse papillomavirus (MmuPV1), produced a protective immune response to this virus. These MmuPV1-exposed mice were less likely to develop skin tumours when their skin was exposed to either (i) the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA), which induces Ras mutations, followed by repeated treatments with a tumour-promoting agent (12-O-tetradecanoylphorbol-13-acetate; TPA); or (ii) DMBA followed by UVB irradiation. On the basis of the results of these experiments, Strickley and colleagues proposed that pre-existing protective immunity to MmuPV1 renders these mice resistant to tumorigenesis at or near to the site of original exposure to the virus. However, the authors did not point out that the skin carcinogenesis protocols used in their animal experiments do not reflect the natural situation in humans. In particular, the experiments on DMBA- and UV-driven skin carcinogenesis were performed by exposing the animals to low doses of UVB (100 mJ cm−2), to avoid local immunosuppression, but it is well established that human skin is exposed to higher and immunosuppressive doses of UVB. In agreement with this, UV exposure in humans is positively associated with multiple markers of β-HPV infection3.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

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

Fig. 1: Model for cooperation between some types of β-HPV and UV radiation in promoting cSCCs.

References

  1. Rollison, D. E., Viarisio, D., Amorrortu, R. P., Gheit, T. & Tommasino, M. An emerging issue in oncogenic virology: the role of beta human papillomavirus types in the development of cutaneous squamous cell carcinoma. J. Virol. 93, e01003-18 (2019).

    Article  CAS  Google Scholar 

  2. Strickley, J. D. et al. Immunity to commensal papillomaviruses protects against skin cancer. Nature 575, 519–522 (2019).

    Article  ADS  CAS  Google Scholar 

  3. Zhao, Y. et al. Cutaneous viral infections associated with ultraviolet radiation exposure. Int. J. Cancer (2020).

  4. Cladel, N. M. et al. Mouse papillomavirus infections spread to cutaneous sites with progression to malignancy. J. Gen. Virol. 98, 2520–2529 (2017).

    Article  CAS  Google Scholar 

  5. Uberoi, A., Yoshida, S., Frazer, I. H., Pitot, H. C. & Lambert, P. F. Role of ultraviolet radiation in papillomavirus-induced disease. PLoS Pathog. 12, e1005664 (2016).

    Article  Google Scholar 

  6. Cladel, N. M. et al. Mouse papillomavirus infection persists in mucosal tissues of an immunocompetent mouse strain and progresses to cancer. Sci. Rep. 7, 16932 (2017).

    Article  ADS  Google Scholar 

  7. Spurgeon, M. E. et al. A novel in vivo infection model to study papillomavirus-mediated disease of the female reproductive tract. MBio 10, e00180-19 (2019).

    Article  CAS  Google Scholar 

  8. Hasche, D. et al. The interplay of UV and cutaneous papillomavirus infection in skin cancer development. PLoS Pathog. 13, e1006723 (2017).

    Article  Google Scholar 

  9. Viarisio, D. et al. E6 and E7 from beta HPV38 cooperate with ultraviolet light in the development of actinic keratosis-like lesions and squamous cell carcinoma in mice. PLoS Pathog. 7, e1002125 (2011).

    Article  CAS  Google Scholar 

  10. Hasche, D., Vinzón, S. E. & Rösl, F. Cutaneous papillomaviruses and non-melanoma skin cancer: causal agents or innocent bystanders? Front. Microbiol. 9, 874 (2018).

    Article  Google Scholar 

  11. Venuti, A., Lohse, S., Tommasino, M. & Smola, S. Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance. Phil. Trans. R. Soc. Lond. B 374, 20180287 (2019).

    Article  CAS  Google Scholar 

  12. Viarisio, D. et al. Beta HPV38 oncoproteins act with a hit-and-run mechanism in ultraviolet radiation-induced skin carcinogenesis in mice. PLoS Pathog. 14, e1006783 (2018).

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA

    Paul F. Lambert

  2. Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA, USA

    Karl Münger

  3. Division of Viral Transformation Mechanisms, German Cancer Research Center (DKFZ), Heidelberg, Germany

    Frank Rösl & Daniel Hasche

  4. Infections and Cancer Biology Group, International Agency for Research on Cancer, World Health Organization, Lyon, France

    Massimo Tommasino

Authors
  1. Paul F. Lambert
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Karl Münger
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Frank Rösl
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Daniel Hasche
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Massimo Tommasino
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

P.F.L., K.M., F.R., D.H. and M.T. contributed to article preparation and approved the submitted version. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy, or views of the International Agency for Research on Cancer/World Health Organization.

Corresponding author

Correspondence to Massimo Tommasino.

Ethics declarations

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Lambert, P.F., Münger, K., Rösl, F. et al. Beta human papillomaviruses and skin cancer. Nature 588, E20–E21 (2020). https://doi.org/10.1038/s41586-020-3023-0

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s41586-020-3023-0

This article is cited by

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.

Search

Advanced search

Quick links

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