Harald zur Hausen links HPV to cervical cancer

Historical milestone — this page describes an event dated 1983. It is not current breaking news.

What zur Hausen did

In the 1970s the dominant view was that cervical cancer was caused by herpes simplex virus. Harald zur Hausen, a German virologist, disagreed. He proposed that human papillomavirus, or HPV, was the cause, and he spent more than ten years trying to prove it.

His key insight was about where to look. He reasoned that if a cancer-causing virus were present, its DNA would be built into the tumor cell's own genome, sitting there in a non-productive state rather than churning out new virus. So instead of hunting for active virus, he searched tumor tissue directly for viral DNA sequences.

The search was hard, because only parts of the viral DNA were integrated. In 1983 he found a new cancer-causing type, HPV16, in cervical tumor biopsies. In 1984 he and his team cloned both HPV16 and HPV18 from patients' cancers. Those two types are consistently found in about 70 percent of cervical cancer samples worldwide.

He was awarded half the 2008 Nobel Prize in Physiology or Medicine "for his discovery of human papilloma viruses causing cervical cancer." The other half went to Françoise Barré-Sinoussi and Luc Montagnier for discovering HIV.

Why finding a cause changed everything

A cancer with a known infectious cause can be attacked at two points that are otherwise closed off. You can stop the infection. And you can look for the cell changes it produces, before they become cancer.

Both of those now exist for cervical cancer, and neither would have been possible without knowing which virus to target.

What HPV actually does

HPV infects squamous cells, the thin flat cells lining surfaces such as the cervix. NCI describes 12 high-risk types: HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59. Types 16 and 18 account for most HPV-related cancers.

Infection itself is extremely common. NCI states that nearly all sexually active people are infected with HPV within months to a few years of becoming sexually active, and around half of those infections involve a high-risk type.

Almost all of those infections are controlled by the immune system and go away. Cancer comes from the exception. When a high-risk infection persists for many years, it can drive cell changes that become precancerous and, if untreated, cancerous.

High-risk HPV infection causes no symptoms. That is precisely why screening exists: there is nothing to notice.

Prevention and screening today

The Gardasil 9 vaccine protects against nine HPV types, including the seven that cause most HPV-related cancers and the two low-risk types behind most genital warts. NCI estimates it can prevent up to 90 percent of cancers caused by HPV infection.

It works best given early, before exposure. NCI says vaccination offers the most protection at ages 9 to 12, and the series is recommended for girls and boys at 11 or 12. Starting before age 15 means two doses; starting at 15 or later means three. Catch-up vaccination is recommended up to age 26. The vaccine is approved through age 45, but is not routinely recommended between 27 and 45, because most people in that range have already been exposed. Our page on the HPV vaccine covers the details.

Screening runs alongside it. NCI lists three tests: an HPV test that checks cervical cells for high-risk types, a Pap test that looks for cell changes, and a co-test that does both. Our page on cervical cancer screening explains the schedules.

When to get checked

• Keep to the cervical screening schedule your clinician recommends. Precancer causes no symptoms, and screening is the only way to find it.
• Ask about the HPV vaccine for children at 11 or 12, or from age 9, and about catch-up doses up to 26.
• Book an appointment for bleeding between periods, bleeding after sex, or any bleeding after menopause.
• Also raise unusual vaginal discharge, or pelvic pain that is new and persistent.
• Attend the follow-up if a screening result is abnormal. An abnormal result is common and usually not cancer, but it needs the next step.

The numbers now

The American Cancer Society projects 13,490 new cervical cancers in the United States in 2026 and 4,200 deaths. In NCI's SEER data, new diagnoses fell by more than 50 percent between 1975 and 2010, largely because screening finds and removes precancerous changes.

About 41 percent are found while still confined to the cervix, 37 percent after spread to nearby lymph nodes and 16 percent after spread further. Five-year relative survival across all stages was 68.8 percent for women diagnosed from 2016 through 2022. About 0.6 percent of women are diagnosed at some point in life.

Those are group statistics about women diagnosed years ago. They describe a population, not a person.

What this finding cannot tell you

• The 1983 date marks HPV16. HPV18 followed, and both were cloned in 1984, so the milestone really spans two years.
• More than 20 years passed between the discovery and the first approved HPV vaccine in 2006, and longer still before vaccination reached most of the world.
• HPV infection is not the same as cancer. Nearly everyone gets HPV; very few get cervical cancer.
• Vaccination does not replace screening. It does not cover every high-risk type, and it does not help with an infection already established.
• This is a summary of a historical event, not advice about anyone's own care.

Our overviews of cervical cancer and HPV and cancer go further into both.

Sources

• https://www.nobelprize.org/prizes/medicine/2008/press-release/
• https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-and-cancer
• https://www.cancer.gov/types/cervical
• https://seer.cancer.gov/statfacts/html/cervix.html

An AI-assisted editorial system helped prepare this page. No named medical reviewer has reviewed it unless one is listed.

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