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The Cancer Vaccine: How Harald zur Hausen Discovered HPV and Won the Nobel Prize

The medical establishment spent a decade convinced that Herpes Simplex Virus was the cause of cervical cancer; Harald zur Hausen proved that a common wart virus—Human Papillomavirus type 16—was the true oncogenic culprit. Awarded the 2008 Nobel Prize in Medicine, this discovery led directly to the Gardasil HPV vaccine, putting humanity on track to eradicate cervical cancer entirely.

Author
Matthias Dürst et al.
Published
1983
Journal
Proceedings of the National Academy of Sciences
Last updated
September 2026
The Cancer Vaccine: How Harald zur Hausen Discovered HPV and Won the Nobel Prize

In the 1970s, cervical cancer was one of the leading causes of cancer death in women worldwide. Medical orthodoxy insisted that Herpes Simplex Virus caused the disease, leading researchers down a dead-end street for over a decade while millions of cancer patients died.

German virologist Harald zur Hausen looked at the DNA of common papillomaviruses that cause skin warts. In 1983, his team isolated and cloned a new viral strain—HPV 16—and discovered its genetic fingerprints embedded inside more than sixty percent of all malignant cervical tumors worldwide.

Zur Hausen’s discovery earned him the 2008 Nobel Prize in Medicine. By proving that cervical cancer was an infectious disease, by inspiring the development of the Gardasil vaccine that prevents over ninety percent of cervical cancers, and by saving hundreds of thousands of lives annually, HPV virology is on track to eliminate a major human cancer.

Reference

Dürst, M., Gissmann, L., Ikenberg, H., & zur Hausen, H. (1983). A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions. Proceedings of the National Academy of Sciences, 80(12), 3812–3815.

Title

A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions.

Abstract

DNA from one biopsy sample of invasive cancer of the cervix contained sequences hybridizing with human papillomavirus (HPV) type 11 DNA only under nonstringent conditions. This DNA was molecularly cloned in lambda phage. Under stringent conditions of hybridization it cross-hybridized to a minor extent (less than 0.1%) with HPV types 10, 14, and 15 and showed no homology with DNA of other human HPV types. We therefore propose to designate it tentatively as HPV 16. HPV 16 DNA was used as a probe to test additional cancer biopsy samples from cervical, vulval, and penile cancer, as well as benign genital warts (condylomata acuminata) and cervical dysplasias for the presence of homologous sequences. In 61.1% (11/18) of cervical cancer samples from German patients sequences were found hybridizing with HPV 16 DNA under conditions of high stringency. In contrast, only 34.8% (8/23) of cancer biopsy samples from Kenya and Brazil revealed this DNA. Vulval and penile cancer biopsy samples hybridized to 28.6% (2/7) or 25% (1/4), respectively. Only 2 out of 33 condylomata acuminata contained HPV 16 DNA. Both positive tumors harbored in addition HPV 6 or HPV 11 DNA. The data thus indicate that HPV 16 DNA prevails in malignant tumors, rendering an accidental contamination with papillomavirus DNA from adjacent papillomas rather unlikely. The rare presence in benign genital papillomas in addition to common genital papillomaviruses suggests a dependence of HPV 16 replication on helper virus.

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