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For five straight years, across the whole of England, not a single woman between the ages of 20 and 24 died of cervical cancer. Run the historical rates forward and you would have expected around 23 deaths in that window. Instead the registers show nothing. A flat, astonishing zero.
Peter Sasieni has spent more than two decades getting to that number. He and Milena Falcaro, both at Queen Mary University of London, have been pulling on the same thread since before most of the women in their data were old enough for secondary school.
The logic ran in three links. HPV causes cervical cancer; vaccination stops the infection; so vaccination should, eventually, stop the dying. The first two were nailed down years ago, in trials and incidence studies. The third was always the hard one, because to show a vaccine prevents death you have to wait for the unvaccinated to die and the vaccinated not to, and that takes a generation. The girls who rolled up their sleeves in school gyms back in 2008 are only now reaching their early thirties.
So the pair did something almost old-fashioned. They went to the national mortality registers and started counting.
Every cervical cancer death in England from 2001 to 2024, sorted into five-year age bands, laid alongside the vaccination coverage for each birth cohort. England makes a near-perfect natural experiment here: the school programme began in 2008 for twelve and thirteen-year-olds, a catch-up campaign swept up older teenagers, and uptake climbed to roughly 90 per cent before the pandemic arrived to complicate everything.
“For more than two decades, our team has been building evidence to show that HPV causes cervical cancer and that vaccination prevents infections, precancerous changes, and the disease itself,” Sasieni says. “This is the first study of the impact of HPV vaccination on cervical cancer mortality.”
Reading death from a coverage chart
Plot the rates by year and they do something striking. For a long stretch they sit more or less flat, drifting up a touch here, down a touch there, the ordinary noise of a rare disease. Then, just as the vaccinated cohorts age into each band, the line falls off a cliff. The timing is the real tell. In each successive five-year age group the drop arrives about five years later, marching upward through the population exactly as the vaccinated women move through it, and that lag is what rules out the boring explanations. A change in treatment would hit every age at once. This doesn’t. It tracks the jab, cohort by cohort, like a tide coming in.
The clever bit, statistically, is that Sasieni and Falcaro never knew which individual women had been vaccinated. They had population coverage and population deaths, nothing more. To pull a per-person effect out of that, Falcaro built a model that treats each age group’s death rate as a blend of two crowds: vaccinated women carrying some unknown relative risk, and unvaccinated women carrying the historical one. Let the maths solve for the unknown.
For women vaccinated at twelve or thirteen, the answer it returns is a risk reduction of 100 per cent, with the lower edge of the confidence interval still sitting north of 80 per cent.
The careful hundred
Sasieni is careful about that hundred, mind. The zero among the youngest women is, the authors write, almost certainly a touch of luck laid over a genuinely tiny underlying risk rather than literal eradication. No vaccine is flawless, and the bivalent jab those early cohorts received covers the two viral types behind most (though not quite all) cervical cancers; roughly nine in ten of the cancers seen in under-thirties in England carry one of them. So the honest reading is not that the risk is nil, but that it has shrunk to something the registers can barely catch. “It is incredible to think that a single jab can almost eliminate a particular type of cancer,” Sasieni says, and the word doing the quiet work in that sentence is almost.
There is a softer result tucked in for the older women, the ones who got the vaccine at fifteen, sixteen, seventeen. Their protection is real but blunter, the reduction shallower and the confidence intervals wide enough to drive a bus through. The reason is uncomfortable biology: by their mid-teens, some had already met the virus, and the vaccine does nothing for an infection you already carry.
Tally the deaths that simply didn’t happen and the running total reaches almost 200 by the close of 2024. As public-health numbers go that is modest, and the authors say so plainly. But it is the leading edge of something that compounds. Cervical cancer mostly kills women in middle age, decades downstream of the infection that seeds it, and the vaccinated cohorts are still young. Every year they grow older, they move into the ages where the disease used to do its real damage, and simply aren’t there to be counted. The prevented deaths, the team reckons, should climb roughly exponentially for the next twenty years.
Which is what gives this otherwise sober register study its strange weight. Cervical cancer remains the second most common cancer killer of women under 65 worldwide, and here is the first hard national evidence, observational but robust, that the central tool actually delivers on the final outcome rather than just the precancers that came before. It lands at the precise moment when uptake is slipping and hesitancy is climbing. The young women who didn’t die didn’t die because nearly nine in ten of their cohort took the vaccine, and that whole result rests on a number now drifting the wrong way. You don’t need the authors to tell you what happens to the next chart if it keeps falling.
https://doi.org/10.1016/S0140-6736(26)00918-9
Frequently Asked Questions
Does this mean the HPV vaccine has wiped out cervical cancer in young women?
Not quite, and the researchers are the first to say so. The five years with zero deaths in 20 to 24-year-olds almost certainly reflect a touch of chance sitting on top of a genuinely tiny risk, rather than the disease being eradicated outright. The fairer reading is that the risk in vaccinated women has shrunk to a level the national registers can barely detect.
Why does the age you get vaccinated matter so much?
The vaccine prevents HPV infection but does nothing about an infection already present. Girls jabbed at twelve or thirteen, before any likely exposure, showed the strongest protection, while those vaccinated at fifteen to eighteen saw a smaller, blunter benefit because some had already encountered the virus. That gap is the strongest argument in the study for vaccinating early.
How can they measure a per-person effect without knowing who was vaccinated?
They couldn’t track individuals, so they used a statistical model that treats each age group’s death rate as a mixture of vaccinated and unvaccinated women and solves for the unknown risk in the vaccinated group. The timing of the decline, arriving five years later in each successive age band as vaccinated cohorts age into it, is what lets them attribute the fall to the vaccine rather than to changes in treatment or screening.
Why does it matter that vaccination rates are now falling?
The entire result rests on coverage reaching nearly 90 per cent in the protected cohorts. With uptake slipping and hesitancy rising, future cohorts may not enjoy the same near-total protection, which would slow or reverse the downward trend in deaths over coming decades. The benefit is expected to grow exponentially for twenty years, but only if coverage holds.
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