On this page
Most of us think of cancer as something that goes wrong inside our own cells. Your NCERT chapter adds a twist: some viruses, called oncogenic viruses, carry genes that can push cells towards cancer. The clearest human example is the link between human papillomavirus (HPV) and cervical cancer, and it was established by Harald zur Hausen after more than a decade of searching. This post covers how he did it, reads the numbers in his key paper, and explains why it led to a vaccine.
Who was Harald zur Hausen?
His Nobel facts page says he was born on 11 March 1936 in Gelsenkirchen, Germany, and died on 28 May 2023 in Heidelberg. He received one half of the 2008 Nobel Prize in Physiology or Medicine "for his discovery of human papilloma viruses causing cervical cancer". The other half went to Francoise Barre-Sinoussi and Luc Montagnier for HIV.
In his Nobel biography he recalls that bombing raids closed his school in 1943, leaving gaps he had to catch up on. He studied medicine, worked on the Epstein-Barr virus in Philadelphia, and then, back in Germany, showed that its DNA persists inside Burkitt's lymphoma cells. That idea, that a virus can hide its DNA inside tumour cells, shaped everything that followed.
Why did he doubt the herpes theory?
In the late 1960s the main suspect for cervical cancer was herpes simplex virus type 2. zur Hausen's biography says his group searched cervical cancer biopsies for its DNA, and "all attempts, however, failed". Meanwhile he had read many case reports of genital warts turning into cancers. Warts are caused by papillomaviruses, so he switched suspects.
The 2008 Nobel press release sums up his reasoning: if tumour cells contained a cancer-causing virus, they should carry viral DNA in their genomes, and that DNA should be found by searching for it directly. The search was hard because only parts of the viral DNA were integrated.
How were HPV 16 and 18 found?
His team first discovered that "papillomavirus" is not one virus but many types. In 1979 his co-workers isolated HPV 6 from genital warts, but it was not in cervical cancers. A related type, HPV 11, gave a weak signal: according to the biography, using HPV 11 as a probe, one of 24 cervical cancer biopsies was positive, and others showed faint bands. Two students, Mathias Durst and Michael Boshart, cloned the DNA behind those faint bands. The results were HPV 16, reported in 1983, and HPV 18, reported in 1984.
Worked example: reading the 1983 paper
The HPV 16 paper, Durst and colleagues in PNAS (1983), tested tumour samples for HPV 16 DNA. Its abstract reports:
Cervical cancers from German patients: 11 of 18 positive.
Cervical cancers from Kenya and Brazil: 8 of 23 positive.
Benign genital warts: 2 of 33 positive.
German samples: 11 / 18 = 0.611, or 61.1%.
Kenya and Brazil: 8 / 23 = 0.348, or 34.8%.
Warts: 2 / 33 = 0.061, or about 6%.
The contrast matters. HPV 16 was common in cancers and rare in harmless warts, so it was unlikely to be a contaminant from nearby warts. The lower rate in samples from Kenya and Brazil hinted that other HPV types were also involved, and HPV 18 turned up the next year in a paper in The EMBO Journal.
What happened inside the cancer cells?
The biography says the viral DNA was usually found integrated into the host DNA, and two viral genes, E6 and E7, were consistently switched on in the cancer cells. This fits the NCERT account in Human Health and Disease: "Cancer causing viruses called oncogenic viruses have genes called viral oncogenes."
There was a setback, too. zur Hausen writes that early approaches to drug companies about a vaccine failed because one market analysis said there would be no market. That changed later.
Why does this matter now?
The WHO cervical cancer fact sheet says cervical cancer is the fifth most common cancer in women, with about 604,000 new cases and 280,000 deaths in 2024. All licensed HPV vaccines protect against HPV 16 and 18, which cause around 76% of cervical cancers. WHO makes vaccinating girls aged 9 to 14 a priority, with one or two doses depending on the national schedule, and also recommends regular screening.
What can a student take from zur Hausen's way of working?
Drop a theory when the evidence does. Years of failed herpes searches told him to look elsewhere.
Turn a hypothesis into a search method. "The DNA should be in the tumour" told him exactly what experiment to run.
Chase the faint signal. One positive out of 24 and a few faint bands were enough to keep going.
For more on how normal cells become cancer cells, read our guide to cancer biology. If oncogenes and proto-oncogenes still feel blurry, the Fermi Concept Library covers every concept in biology, each with its own lesson and its place in the map.
Try it now: explain in three sentences why finding HPV 16 in warts only 2 times out of 33 strengthened the case that it causes cancer.
