One Virus, Two Cancers: What HPV in the Throat Has in Common With HPV in the Cervix

Most people have heard that the human papillomavirus (HPV) causes cervical cancer. Far fewer know that the same virus is now one of the leading causes of throat cancer, and that infections in both parts of the body are transmitted, and switch on cancer, in strikingly similar ways. As Ghana rolls out its first nationwide HPV vaccination campaign for adolescent girls, it is worth understanding why this one virus deserves attention well beyond the cervix.

A virus with more than 200 faces

HPV is not a single virus but a family of more than 200 related viruses that infect skin and mucous membranes. Most types are harmless and clear on their own within one to two years. A smaller group, classified as "high-risk" types, can persist in the body and gradually push infected cells toward cancer. Two of these, HPV-16 and HPV-18, are responsible for the majority of HPV-related cancers worldwide, including most cervical cancers and a large share of oropharyngeal (throat) cancers.

HPV spreads through direct skin-to-skin and mucosal contact during vaginal, anal, and oral sex. It does not require the exchange of bodily fluids the way HIV or hepatitis B does, which is part of why it is the most common sexually transmitted infection globally, and why condoms, though protective, do not eliminate risk entirely since they don't cover all exposed skin.

Oral sex: the specific route into the throat

Because oropharyngeal cancer is the less familiar of the two diseases, it is worth being precise about how HPV actually gets into the throat, since the evidence here comes from some of the largest behavioural studies conducted on the subject.

The clearest data come from a landmark U.S. case-control study led by epidemiologist Gypsyamber D'Souza and colleagues, which compared 100 patients with oropharyngeal cancer to 200 matched cancer-free controls. Among the patients with cancer, 88 percent reported having had at least one lifetime oral-sex partner, and oral HPV-16 infection was found in 32 percent of cancer patients versus just 4 percent of controls, while any oral HPV infection was found in 37 percent of patients versus 6 percent of controls. That study was central to establishing oral sex, specifically, rather than sexual activity in general, as a driver of this cancer.

A larger follow-up study by the same research group, published in 2021 and covering 163 oropharyngeal cancer patients and 345 matched controls, found that people with more than 10 lifetime oral-sex partners had over four times the odds of developing HPV-related oropharyngeal cancer compared with those with fewer partners. The same study found that starting oral sex before age 18, having oral sex with partners at least ten years older, and having a higher "intensity" of oral-sex partners over a short period were each independently linked to higher risk, on top of partner count alone.

National survey data collected in the United States (NHANES) similarly show a clear gradient: oral HPV was found in fewer than 2.5 percent of people who reported never having performed oral sex, rising to as much as 14 to 15 percent among men who had both smoked and had five or more lifetime oral-sex partners. Across that same national dataset, men were roughly six times more likely than women to carry oncogenic oral HPV, which lines up with the fact that HPV-related throat cancer affects men several times more often than women worldwide.

None of this means oral sex is unusually dangerous compared to other forms of sexual contact, or that people who have had oral sex will develop cancer; the great majority of oral HPV infections, like cervical ones, clear on their own. What the data show is a dose-response relationship: the more lifetime oral-sex exposure to HPV a person has, particularly starting at a younger age or with more partners, the higher their cumulative risk of a persistent infection that could, over decades, progress to cancer.

The same molecular hijack, two different addresses

What links cervical cancer and HPV-driven throat cancer is not just the virus's name, but its precise mechanism of harm. When a high-risk HPV type infects the basal cells of the cervix or the tissue lining the tonsils and base of the tongue, it produces two small viral proteins, E6 and E7, that hijack the host cell's own safety systems.

Ordinarily, a cell has built-in checkpoints that stop damaged or abnormally dividing cells from surviving and multiplying. The E6 protein binds to and marks for destruction a tumour-suppressor protein called p53, often described as the "guardian of the genome," which would otherwise force damaged cells to stop dividing or self-destruct. Around the same time, the E7 protein disables another checkpoint protein, the retinoblastoma protein (Rb), which normally keeps cells from dividing until they are ready. With both brakes released, infected cells are pushed to keep dividing even as genetic damage accumulates, and cells that should have died instead survive, replicate, and can eventually pass this instability on to daughter cells. Over years, this can progress from precancerous changes to invasive cancer.

Because this E6/E7 mechanism is the same whether the infected tissue is cervical epithelium or the lymphoid tissue of the tonsils and tongue base, HPV-driven cervical cancer and HPV-driven oropharyngeal cancer are, at the molecular level, closely related diseases arising in different organs.

Where the two cancers diverge

Despite the shared mechanism, the two cancers differ in important ways that matter for prevention and detection.

Cervical cancer overwhelmingly affects women and has a well-established screening pathway: Pap smears and HPV DNA tests can catch precancerous cervical changes years before they become cancer, which is why organised screening programmes have driven down cervical cancer rates wherever they have been sustained.

HPV-related oropharyngeal cancer, by contrast, disproportionately affects men, and there is no equivalent routine screening test for the throat. Research tracking cancer registries has found that HPV-positive throat cancers have risen sharply in higher-income countries over the past two decades, even as tobacco-related throat cancers have declined, so that HPV is now estimated to cause a majority of oropharyngeal cancers in some developed countries. Because there is no early-warning test, these cancers are often diagnosed only after a person notices a persistent sore throat, difficulty swallowing, an unexplained lump in the neck, or ear pain that does not resolve, symptoms easy to dismiss until the disease is more advanced.

As the data above show, risk rises specifically with the number and pattern of oral-sex partners, and is compounded further by smoking and a weakened immune system, all of which make it harder for the body to clear a persistent high-risk HPV infection before it can trigger these changes.

The burden, in numbers

Cervical cancer remains the fourth most common cancer in women globally, with roughly 660,000 new cases and 350,000 deaths a year, around 90 percent of them in low- and middle-income countries. In Ghana specifically, there were an estimated 3,072 new cervical cancer cases in 2023. Across sub-Saharan Africa, the burden is especially heavy: the region records well over 117,000 new cervical cancer cases and more than 76,000 deaths annually, the highest incidence of any region in the world, largely because screening and vaccination coverage have historically lagged behind higher-income countries.

Throat cancer's HPV story is a more recent one. Global estimates attribute roughly 30 to 43 percent of oropharyngeal cancers to HPV infection, with some high-income countries reporting figures well above that. In the United States, HPV-positive throat cancer cases rose by more than 200 percent between 1988 and 2004, and HPV is now believed to cause around 70 percent of oropharyngeal cancers in similar developed-country settings. Men are consistently affected several times more often than women.

Why this matters for Ghana right now

In October 2025, Ghana Health Service, together with Gavi, the WHO, and UNICEF, launched the country's first nationwide HPV vaccination campaign, aiming to reach about 2.4 million girls aged 9 to 14 with a vaccine that is now being folded into the routine immunisation schedule. This is expected to prevent tens of thousands of future cervical cancer deaths, and it lines up Ghana with the WHO's global target of eliminating cervical cancer as a public health problem by pushing incidence below 4 cases per 100,000 women.

What is less discussed locally is that the same vaccine also protects against the HPV types responsible for most throat cancers, and current guidance supports vaccinating boys as well as girls, since men bear a disproportionate share of the HPV-related throat cancer burden and unvaccinated men also continue to transmit the virus. A vaccination conversation framed only around "protecting girls from cervical cancer" leaves out half the picture, and half the population that could benefit.

What actually works

The core prevention message is genuinely simple, even if the biology behind it is complex:

• Get the HPV vaccine, ideally before the start of sexual activity, since it works best before a person is exposed to the virus. In Ghana, this is now free for eligible girls through the national programme.
• Attend cervical screening on the recommended schedule if you are a woman old enough to be eligible; it remains the only proven way to catch cervical changes before they become cancer.
• Practise safer sex, including barrier protection during oral sex and being mindful that risk rises with the number of oral-sex partners and with starting oral sex at a younger age, recognising that barrier methods reduce but do not eliminate risk.
• Avoid smoking, which independently increases the risk of HPV-related cancers and appears to make it harder for the body to clear persistent infection.
• Take unexplained, persistent throat or neck symptoms seriously and seek medical evaluation, since there is no routine screening test to catch HPV-related throat cancer early the way a Pap smear can for cervical cancer.

A shared virus deserves a shared conversation

Cervical cancer and HPV-related throat cancer are often discussed as though they belong to entirely separate conversations, one about women's reproductive health, the other barely discussed at all. But they are driven by the same virus, using the same molecular playbook, and they respond to the same core prevention tools: vaccination, informed sexual health choices, and not smoking. As Ghana pushes forward with its HPV vaccination campaign, broadening the public conversation to include throat cancer, and to include boys and men, could close a gap in awareness before it becomes a gap in survival.

References

1. World Health Organization. (2020). Global strategy to accelerate the elimination of cervical cancer as a public health problem. WHO. https://www.who.int/publications/i/item/9789240030824

2. World Health Organization. Cervical Cancer Elimination Initiative. https://www.who.int/initiatives/cervical-cancer-elimination-initiative

3. Gavi, the Vaccine Alliance. (2025, October 8). Ghana launches HPV vaccine to protect over 2 million girls and combat cervical cancer. https://www.gavi.org/news/media-room/ghana-launches-hpv-vaccine-protect-over-2-million-girls-and-combat-cervical-cancer

4. International Agency for Research on Cancer (IARC). Elimination Planning Tool: Advancing Towards Cervical Cancer Elimination – Ghana. Global Cancer Observatory. https://gco.iarc.fr/media/elimination_tool/factsheets/288-GHA-ghana.pdf

5. WHO Regional Office for Africa. Kenya launches national cervical cancer elimination action plan 2026–2030. https://afro.who.int/countries/kenya/news/kenya-launches-national-cervical-cancer-elimination-action-plan-2026-2030

6. Obanya, D. I., Wootton, L. M., & Morgan, E. L. (2025). Advances in understanding the mechanisms of the human papillomavirus oncoproteins. Biochemical Society Transactions, 53(3), 565. https://portlandpress.com/biochemsoctrans/article/53/03/565/236056/

7. Fused toes homolog, a potential molecular regulator of HPV16 E6 and E7 oncoproteins in cervical cancer. PMC9009596. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009596/

8. Human Papillomavirus-Associated Oropharyngeal Cancer: Global Epidemiology and Public Policy Implications. (2023). Cancers, 15(16), 4080. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10452639/

9. Epidemiological Trends in the Characterization of Human Papillomavirus Virus-Related Oropharyngeal Cancer: A Global Perspective. (2025). Current Oncology Reports. https://link.springer.com/article/10.1007/s11912-025-01656-4

10. Trends in Oropharyngeal Cancer Incidence Among Adult Men and Women in the United States From 2001 to 2018. PMC9339703. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9339703/

11. Global burden of oropharyngeal cancer attributable to human papillomavirus by anatomical subsite and geographic region. ScienceDirect. https://www.sciencedirect.com/science/article/abs/pii/S1877782122000455

12. HPV cancer burden by anatomical site, country, and region in 2022. (2025). Scientific Reports. https://www.nature.com/articles/s41598-025-06700-8

13. Yeates, K., et al. (2026). Cervical cancer elimination in Africa: Vaccination progress, HPV testing and the promise of AI-assisted triage tools for screening. Open Access Government, April 2026, pp. 140–141. https://www.openaccessgovernment.org/article/cervical-cancer-elimination-in-africa-vaccination-progress-hpv-testing-and-the-promise-of-ai-assisted-triage-tools-for-screening/207704/

14. Ghana Health Service / Africa Health Observatory. 2023 STEPS Survey Findings – Cervical Cancer Screening. https://files.aho.afro.who.int/afahobckpcontainer/production/files/Cervical_Cancer.pdf

15. International Vaccine Access Center (IVAC), Johns Hopkins Bloomberg School of Public Health. (2023–2024). HPV Vaccine Progress and Next Steps for Advocacy in Ghana. https://publichealth.jhu.edu/sites/default/files/2024-02/hpv-vaccine-advocacy-in-ghanaivac2023ax.pdf

16. D'Souza, G., et al. Case-control study establishing oral sexual behaviour as a risk factor for HPV-related oropharyngeal cancer. Summarised in: Is High-Risk Sexual Behavior a Risk Factor for Oropharyngeal Cancer? PMC10340603. https://pmc.ncbi.nlm.nih.gov/articles/PMC10340603/

17. Drake, V. E., et al. (2021). Timing, number, and type of sexual partners associated with risk of oropharyngeal cancer. Cancer. https://doi.org/10.1002/cncr.33346 open-access version: https://pmc.ncbi.nlm.nih.gov/articles/PMC8035131)

18. Number of Sexual Partners, Smoking Identified as Risk Factors for Oropharyngeal Cancer (NHANES analysis). OncLive. https://www.onclive.com/view/number-of-sexual-partners-smoking-identified-as-risk-factors-for-oropharyngeal-cancer

   Comments5