Things to Remember
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HPV is extremely common: About 1 in 7 Americans currently has HPV, and most sexually active adults will get it at some point. Most infections clear on their own within 1-2 years without you ever knowing, but some stick around and can lead to cancer years or even decades later.
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HPV causes multiple types of cancer: While most people know HPV causes cervical cancer, it also causes throat, anal, and other cancers. In fact, HPV-related throat cancer is now more common in the US than cervical cancer, and it mostly affects men.
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The vaccine actually prevents cancer: The HPV vaccine works by teaching your immune system to recognize and block the virus before it can infect you. It prevents about 90% of HPV-related cancers by targeting the most dangerous virus strains - this is real cancer prevention, not just treatment after you're sick.
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It works best before exposure: The vaccine is most effective when given before someone becomes sexually active (typically ages 11-12), but it's approved up to age 45. If you've never been infected with the HPV types in the vaccine, you can still benefit from getting vaccinated.
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The protection is powerful: Studies show the vaccine is about 96% effective at preventing precancerous changes caused by the HPV types it covers. Real-world data from countries with high vaccination rates show dramatic drops in HPV infections and precancerous cervical changes.
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There's no cure for HPV itself: Once you're infected, your body either clears it on its own or it doesn't - there's no medication to treat the virus. This makes prevention through vaccination especially important, since we can only treat the cell changes and cancers that result from persistent infection, not the virus itself.
This article explains what HPV vaccines protect against, who should get them, and why they're one of the most effective cancer prevention tools we have.
Most people think HPV is rare. Or that it's something other people get. The reality is different, and I think we should probably talk about it more openly than we do.
HPV Vaccine Types - Coverage and Key Differences
| Vaccine | HPV Types Covered | Cancers Prevented | Age Approved | Doses Required |
|---|---|---|---|---|
| Gardasil 9 (current standard) | 9 types: 16, 18, 31, 33, 45, 52, 58 (cancer-causing) + 6, 11 (genital warts) | Cervical, oropharyngeal, anal, vaginal, vulvar, penile cancers + ~90% of genital warts | Ages 9-45 | 2 doses (ages 9-14); 3 doses (ages 15+) |
| Gardasil (original, discontinued 2016) | 4 types: 16, 18 (cancer-causing) + 6, 11 (genital warts) | ~70% of cervical cancers, other HPV cancers, ~90% of genital warts | Ages 9-26 | 3 doses over 6 months |
| Cervarix (discontinued in US 2016) | 2 types: 16, 18 (cancer-causing only) | ~70% of cervical cancers, other HPV-16/18 cancers | Ages 9-25 | 3 doses over 6 months |
Top 6 HPV-Related Cancers and Their Risk Profiles
- Cervical Cancer
- HPV attribution: ~91% caused by HPV (primarily types 16 and 18)
- Annual US cases: ~11,500 new diagnoses
- Prevention: Vaccination + regular Pap/HPV screening
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Most affected: Women ages 35-44
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Oropharyngeal Cancer (throat/tonsil/base of tongue)
- HPV attribution: ~70% caused by HPV (primarily type 16)
- Annual US cases: ~19,000 (now exceeds cervical cancer)
- Prevention: Vaccination (no screening test available)
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Most affected: Men ages 50-69
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Anal Cancer
- HPV attribution: ~91% caused by HPV
- Annual US cases: ~8,300
- Prevention: Vaccination + screening for high-risk groups
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Most affected: Women, men who have sex with men, immunocompromised individuals
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Vaginal Cancer
- HPV attribution: ~75% caused by HPV
- Annual US cases: ~1,000
- Prevention: Vaccination + cervical cancer screening may detect early changes
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Most affected: Women over 60
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Vulvar Cancer
- HPV attribution: ~69% caused by HPV
- Annual US cases: ~6,000
- Prevention: Vaccination (screening not routine)
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Most affected: Women over 65
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Penile Cancer
- HPV attribution: ~63% caused by HPV
- Annual US cases: ~2,200
- Prevention: Vaccination (screening not available)
- Most affected: Men over 55
Human papillomavirus - the virus behind most cervical cancers and a growing proportion of throat cancers - is the most common sexually transmitted infection worldwide. In the US alone, an estimated 42 million people are currently infected with a disease-causing type of HPV. That's roughly one in seven people. Every year, about 13 million more get infected. Most of them will never know.
I mention this not to alarm anyone, but because there's something unusual happening here: we have a vaccine that actually prevents cancer. Not treats it after the fact. Prevents it. And yet uptake remains lower than almost every other childhood vaccine we routinely give.
The Virus Itself
HPV is a DNA virus - technically from the Papillomaviridae family, though that detail matters less than what it does. It's transmitted through skin-to-skin genital contact, which makes it nearly ubiquitous among sexually active adults. More than 200 different HPV types have been identified. At least 12 of them are oncogenic, meaning they've been associated with cancer development. That doesn't mean every infection leads to cancer. Far from it. But it does mean the risk exists.
About 90% of new HPV infections become undetectable within one to two years. The immune system clears them. They disappear, and the person moves on without ever knowing they were infected. The problem is the 10% that don't clear. These persistent infections - particularly with high-risk types like HPV16 and HPV18 - can progress to precancerous lesions and, eventually, invasive cancer.
Worldwide, HPV16 and HPV18 account for roughly 70% of cervical cancers. For other HPV-related cancers - throat, anal, vaginal, vulvar, penile - the percentage is even higher. HPV16 alone is responsible for the majority of oropharyngeal cancers, which are now more common in the US than cervical cancer. Most of those cases occur in men.
I still find it striking how few people know this. The association between HPV and cervical cancer is well-known now. The link to throat cancer is less so. But the numbers are clear: in the US, oropharyngeal cancer has become the most common HPV-attributable cancer, and the incidence continues to rise.
How Infection Becomes Cancer
The progression from virus to cancer isn't immediate. It takes years, sometimes decades. The virus first infects the basal epithelial cells - often at the junction between the endocervix and ectocervix, a spot where the epithelium is thin and vulnerable. Any disruption in the epithelial surface - microtrauma during sexual contact, for instance - gives the virus access to the cell and, from there, to the nucleus.
Once inside the nucleus, certain high-risk HPV types can integrate into the host genome. This is where the trouble starts. The viral DNA interferes with normal cell replication and division, particularly by disrupting tumor suppressor genes like p53 and Rb (retinoblastoma protein - proteins that normally prevent unchecked cell growth). Infected cells multiply uncontrollably. Over time, this leads to dysplasia - abnormal cell growth - which can progress to high-grade precancerous lesions and, eventually, invasive cancer.
The timeline varies. Some patients develop high-grade dysplasia - cervical intraepithelial neoplasia (CIN, a classification system for precancerous changes in cervical cells) grade 2 or 3 - within a few years. Others never progress at all. Immunocompromised patients, smokers, and those infected with particularly aggressive HPV subtypes are at higher risk. But even among immunocompetent non-smokers, the risk exists.
Most HPV-related cancers take years to develop. This is why screening works. We can catch precancerous changes early, treat them, and prevent progression to invasive disease. Cervical cancer is currently the only HPV-related cancer with an approved screening protocol, which involves HPV testing, cervical cytology (examination of cervical cells under a microscope to detect abnormalities), or both. If abnormalities are detected, further evaluation - including colposcopy (a procedure where a magnifying instrument examines the cervix) and biopsy - can identify high-grade lesions before they become cancer.
There's no treatment for the virus itself. Once someone is infected, the immune system either clears it or it persists. If it clears, the person is no longer at increased risk for cervical cancer, though the infection can reactivate later. If it persists, close surveillance and management of precancerous lesions become critical.
The Vaccine: How It Works and What It Prevents
HPV vaccines are based on virus-like particles, or VLPs - small protein structures that mimic the outer shell of the virus but contain no genetic material. They can't cause infection. What they can do is trigger an immune response that produces antibodies against the virus. If someone is later exposed to HPV, those antibodies recognize and neutralize the virus before infection can establish itself.
The first HPV vaccines were licensed in 2006 and 2009. They targeted two or four HPV types, respectively. In 2014, a nine-valent vaccine was introduced, covering seven oncogenic strains (including HPV16 and HPV18) plus two non-oncogenic strains that cause genital warts. These seven cancer-causing strains account for approximately 90% of all HPV-attributable cancers worldwide. The nine-valent vaccine is now the only one distributed in the US.
The efficacy data are striking. International randomized controlled trials involving female participants aged 15 to 26 showed vaccine efficacy of at least 96% for preventing cervical precancers caused by vaccine-targeted HPV types. That's in per-protocol populations - meaning participants who had no evidence of infection at the time of vaccination and who received all three doses. Trials of the quadrivalent vaccine demonstrated 100% efficacy for preventing external anogenital, vaginal, and cervical lesions when given prior to HPV exposure.
Subsequent studies in children aged 9 to 15 found that antibody levels following vaccination were non-inferior to - or even higher than - those in the adult trials that demonstrated efficacy. Similar results have been seen in men. Long-term follow-up in Nordic countries showed no cases of HPV16 or HPV18-attributable cervical precancers over 12 years post-vaccination.
What's particularly interesting is that vaccination produces higher antibody titers than natural infection. The immune response to the vaccine is stronger and more durable than the response to the virus itself. This is unusual. For most infections, natural immunity is considered superior. Not here.
Timing Matters: Why Vaccination Before Exposure Is Critical
The vaccine doesn't work once infection is established. It's preventive, not therapeutic. This means it must be given before someone is exposed to the HPV strains covered by the vaccine. Since HPV is transmitted through skin-to-skin genital contact, the vaccine should ideally be given before the onset of any sexual activity.
This is why the recommended age for vaccination is 11 to 12 years, though it can be initiated as early as age 9. At this age, most children haven't been exposed to HPV. The vaccine is maximally effective. There's also a practical benefit: children who receive the vaccine before age 15 require only two doses, spaced six to twelve months apart. Those aged 15 or older need three doses to complete the series. Immunocompromised individuals need three doses regardless of age.
Vaccination is recommended for everyone up to age 26. For people aged 27 to 45, the decision becomes more nuanced. The vaccine may still provide benefit, but by this age, many people have already been exposed to at least some of the HPV types covered by the vaccine. The potential benefit is lower. Shared decision-making between patient and provider is recommended.
I've had this conversation many times. The usual question is: "Is it worth it at my age?" And the answer depends. If someone has had few sexual partners, if they're in a long-term monogamous relationship with a previously unvaccinated partner, if they're starting a new relationship after a period of abstinence - there may still be benefit. But the data are less clear, and the decision is more individual.
Safety and Post-Licensure Surveillance
There's extensive evidence regarding the safety of these vaccines. More than 135 million doses of HPV vaccine have been distributed in the US through 2021. Post-licensure monitoring - both in the US and internationally - has detected no safety concerns beyond rare allergic reactions. Large population-based studies have shown no increased risk of death, autoimmune conditions, or neurologic conditions following vaccination.
This is important to emphasize. Vaccine hesitancy around HPV vaccination remains surprisingly high, often driven by misinformation about safety. The data are clear: the vaccine is safe. The risks of HPV infection and subsequent cancer far outweigh the risks of vaccination.
Real-World Impact: What We've Seen Since Introduction
Twelve years after the US HPV vaccination program launched, the prevalence of vaccine-type HPV infections had decreased by 88% among adolescents aged 14 to 19 and by 81% among those aged 20 to 24. This is remarkable. Even more striking is the herd immunity effect: HPV prevalence has dropped even among unvaccinated individuals. This suggests that widespread vaccination reduces transmission at a population level.
While randomized trials haven't been long enough to directly assess impact on cervical cancer rates, epidemiological data from several countries have shown reduced cervical cancer incidence in vaccinated cohorts. In Scotland, for example, women who received the vaccine between ages 12 and 13 showed an 89% reduction in cervical cancer rates compared to unvaccinated women. Similar trends have been observed in Sweden, Finland, and Australia.
We're starting to see what prevention looks like at scale.
The Gap: Where We Are Now
Despite this, uptake remains lower than it should be. In 2023, 76.8% of US adolescents aged 13 to 17 had received at least one dose of HPV vaccine. Only 61.4% were fully up to date with the recommended series. Compare this to other vaccines routinely given to adolescents - like the meningococcal or Tdap vaccines - where coverage approaches 90%.
I'm not entirely sure why the gap persists. Part of it may be discomfort around discussing a sexually transmitted infection with children. Part of it may be misinformation about vaccine safety. Part of it may simply be that parents don't fully understand what's being prevented. Cancer feels distant when your child is 11. It's abstract. Throat cancer twenty years from now doesn't feel as immediate as meningitis or whooping cough.
But the reality is that this vaccine prevents cancer. Not all cancers, but a meaningful subset. And the evidence is clear: it works best when given early, before exposure.
What This Means Going Forward
HPV vaccination is one of the most effective cancer prevention tools we have. It's safe. It's well-studied. It prevents not just cervical cancer but also oropharyngeal, anal, vaginal, vulvar, and penile cancers. The benefit is greatest when given before exposure, which is why routine vaccination at ages 11 to 12 is recommended.
For those who missed vaccination in childhood, catch-up vaccination up to age 26 is still recommended. Beyond that, the decision becomes more individual. But the principle remains: vaccination before exposure provides the most benefit.
I think we should talk about this more openly than we do. HPV infection is common. The vaccine is effective. The barriers to uptake - whether discomfort, misinformation, or simple lack of awareness - are surmountable.
Some days I wonder if we've gotten too comfortable with the idea that cancer is inevitable. That it just happens. But this is one cancer we can actually prevent. Not all of them, but enough to matter. I think that's worth paying attention to.
