HPV and Cervical Cancer

Contents

1. A large family with a few dangerous members
2. The link was found in the 1980s
3. Most infections clear, a few persist
4. How the changes are found and graded
5. Where the evidence is strongest

Human papillomavirus takes its name from the papilloma, an old word for a wart, built on the Latin papilla, a small swelling, and the colposcopy and LEEP procedures in Candace Cooley’s office based experience exist largely to find and remove the cervical changes this virus causes. The name points at the harmless side of the family. The types that matter for cancer cause no warts and no symptoms at all, and for decades nobody suspected them.

A large family with a few dangerous members

The National Cancer Institute describes HPV as a group of more than 200 related viruses. The sexually transmitted types fall into two groups: low risk types, which rarely cause cancer but can cause genital warts, and 12 high risk types, of which HPV 16 and HPV 18 are responsible for most HPV related cancers.¹ The American College of Obstetricians and Gynecologists notes that those same two types cause most cases of cervical cancer.³

The virus reaches beyond the cervix. The NCI attributes virtually all cervical cancer to HPV, along with most anal, vaginal, vulvar, penile and oropharyngeal cancers, and estimates that it causes about 690,000 cancers a year worldwide.¹ It passes through intimate skin to skin contact, and condoms lower the chance of transmission without preventing it completely. The virus infects the thin, flat squamous cells lining these organs, so most HPV cancers are squamous cell carcinomas, although some cervical cancers arise from glandular cells and are called adenocarcinomas.¹

Figure

Share of cancers caused by HPV, by site

• Penile63
• Vulvar69
• Oropharyngeal70
• Vaginal75
• Anal90

The link was found in the 1980s

Before the 1980s researchers argued over whether hormones, toxins or other factors caused cervical cancer. Our World in Data recounts how Harald zur Hausen’s team, studying viruses then known for causing warts, found HPV DNA integrated into cervical cancer cells, work that later earned a Nobel prize.⁶ The virus damages proteins such as p53 that normally stop cells with harmful mutations from multiplying.⁶ The NCI Center for Cancer Research adds that laboratory and population studies made the link between specific HPV types and cervical cancer increasingly clear through that decade, and identified two viral genes, E6 and E7, whose proteins can together make human cells cancerous.⁴

Most infections clear, a few persist

Infection is close to universal. The NCI states that nearly all sexually active people acquire HPV within months to a few years, about half of them with a high risk type, and that the immune system usually clears the infection within a year or two.¹ A 2025 Oregon study on PubMed Central notes that among patients under 25, as many as 44 percent may see the infection regress without treatment.⁵

Figure

From infection to cancer

1. 01
   InfectionMost sexually active people acquire HPV within months to a few years.
2. 02
   ClearanceThe immune system usually clears the infection within a year or two.
3. 03
   PersistenceIn a minority, a high risk infection lasts for years.
4. 04
   PrecancerPersistently infected cells can become precancerous in about 5 to 10 years.
5. 05
   CancerUntreated precancer can become cancer, typically about 20 years after infection.

The danger lies in persistence. When a high risk infection lasts for years it can produce cell changes that worsen into precancer and then cancer; the NCI puts the interval at 5 to 10 years to precancer and about 20 years to cancer.¹ Factors that make persistence more likely include an aggressive type, particularly 16 or 18, smoking, HIV and other causes of a weakened immune system.¹ A high risk infection itself causes no symptoms. Only the precancers and cancers it produces, years later, may bring lumps, bleeding or pain, which is why screening rather than symptoms finds most cases early.¹

How the changes are found and graded

ACOG explains that cells infected with HPV look different under the microscope, and that biopsy results are reported as cervical intraepithelial neoplasia, graded 1 to 3. CIN 1 is a mild change that usually goes away without treatment, while CIN 2 and CIN 3 are high grade changes that can progress to cancer.³ High grade changes are usually treated by removing tissue, most often with a LEEP, or by destroying it with freezing or laser.³ The examination that leads to those biopsies is described in the entry on colposcopy. After an abnormal screening result, ACOG lists the usual next steps: reflex testing on the same sample, typing for HPV 16 and 18, repeat testing, or colposcopy, chosen according to age and earlier results, with an HPV test recommended six months after any treatment.³

The two screening tests ask different things. In the Oregon study, which reviewed more than 22,000 tests, HPV testing caught a slightly larger share of high grade lesions than cytology but was less specific, returning more positive results in women whose biopsies proved normal, and neither test caught every case.⁵ How guidelines have weighed those tradeoffs is traced in how cervical screening guidelines changed.

Figure

Cytology and HPV testing in one Oregon study

	Cytology (Pap test)	HPV test
What it examines	Cervical cells under the microscope	Genetic material of high risk HPV types
Sensitivity for CIN 2 or worse	78.3%	88.8%
Specificity for CIN 2 or worse	48.9%	27.1%
CIN 3 cases with an abnormal result	82.9%	90.6%

Where the evidence is strongest

The causal chain from persistent high risk HPV to cervical cancer is the best established part of the story, and the NCI calls the virus the cause of virtually all cases.¹ Close behind is the evidence that vaccines prevent the infections and precancers that lead to it. The Centers for Disease Control and Prevention states that the vaccine protects against the types behind most cervical cancers, and that screening with follow up treatment can prevent the disease or find it early.²

Evidence on deaths is newer and population based. CIDRAP reported a 62 percent fall in cervical cancer deaths among American women under 25 over a decade, which the researchers linked to vaccination.⁹ The Guardian reported a 2026 English study finding that no women aged 20 to 24 died of the disease there between 2020 and 2024.⁷ A commentary described by EurekAlert cautioned that such data cannot alone prove cause and effect, since screening and herd immunity also played a part, and that vaccinated groups must be followed into older ages.⁸ The burden remains heavy elsewhere: Our World in Data counts more than 660,000 new cases and about 350,000 deaths worldwide in 2022, concentrated where screening is scarce and HIV common.⁶ The same source reports that in England’s youngest vaccinated group, cervical cancer rates were about 87 percent lower than in the oldest unvaccinated groups.⁶ What any one woman’s results mean for her is best worked through with her own clinician; the prevention side of the story continues in the entry on the HPV vaccine.