HPV: From Infection to Warts, Screening and Cancer Risk

A 22-year-old woman attends a sexual health service after noticing several small, painless raised lesions around the vulva. They have been present for a few weeks and are not particularly uncomfortable, but she is frightened that they might be cancer. During the consultation she asks whether this means her partner has given her a “cancer-causing HPV”.

Elsewhere in primary care, a 29-year-old receives her cervical-screening result. High-risk human papillomavirus (HPV) has been detected, but no abnormal cell changes have been found. She is equally worried and asks whether a positive HPV result means she is developing cervical cancer.

These two patients help us understand one of the most important things about HPV: HPV is not one virus, and genital warts and HPV-associated cancer are not the same disease process.

What might their results and symptoms suggest?

The first patient's lesions may be anogenital warts. Around 90% are caused by HPV types 6 and 11. These are described as low-risk HPV types because they are not the types responsible for most HPV-associated cancers. Warts are benign epithelial growths and may be soft and papillomatous, papular, flat or keratotic. They can occur on genital or perianal skin and on mucosal surfaces. (BASHH, 2024)

The second patient has a different issue. Her screening sample contains a high-risk HPV type. High-risk types can persist within epithelial tissue and contribute to precancerous cell changes and, in a minority of persistent infections, cancer. HPV 16 and 18 are particularly important oncogenic types. A positive high-risk HPV result is therefore a marker of increased risk that needs the appropriate screening pathway. It is not a diagnosis of cancer.

HPV is extremely common. Public Health Scotland notes that most people will acquire some type of HPV during their lifetime, usually without knowing because infection commonly causes no symptoms. (Public Health Scotland)

What is happening and why?

HPV is a DNA virus with a particular relationship with epithelium, the layers of cells covering skin and mucosal surfaces. The virus reaches basal epithelial cells through tiny breaks or micro-abrasions. Once inside, its life cycle becomes linked to the normal maturation of epithelial cells. Viral DNA is maintained in infected basal cells, and as their daughter cells move upwards and differentiate, viral replication and production of new viral particles can occur nearer the epithelial surface.

This helps explain several features of HPV. It can remain localised in skin or mucosa rather than producing a bloodstream infection, and viral particles can be present at the surface even when there is no visible lesion. Transmission therefore occurs mainly through direct intimate skin-to-skin contact and does not require penetrative sex. Condoms reduce exposure but cannot cover every potentially infected area of genital skin.

Why do some HPV types cause warts while others are associated with cancer?

Low-risk HPV types stimulate epithelial proliferation in a way that can produce the visible growth we recognise as a wart. The lesion itself is benign. BASHH notes that oncogenic HPV types can occasionally coexist within wart tissue, but the HPV types responsible for typical anogenital warts are not the main drivers of anogenital cancer. (BASHH, 2024)

High-risk HPV behaves differently when infection persists. Two viral proteins, E6 and E7, interfere with normal cell-cycle safeguards. E6 promotes degradation of the tumour-suppressor protein p53, which normally helps stop damaged cells dividing or directs them towards apoptosis when damage is severe. E7 disrupts the retinoblastoma protein (pRb) pathway, allowing cells to move through the cell cycle when they would normally be held back. Persistent disruption of these controls can allow abnormal cells to survive and accumulate further genetic changes.

This process takes time. Most high-risk HPV infections do not become cancer. The concern is persistent infection accompanied by progressive epithelial abnormality over years. Smoking, immune suppression and other cofactors can increase the likelihood of persistence or progression. High-risk HPV is associated with cervical, anal, penile, vulval, vaginal and some oropharyngeal cancers. In Scotland, HPV 16 and 18 are responsible for around 80% of cervical cancers. (Public Health Scotland)

What else would you want to know?

For the patient with possible warts, establish when the lesions appeared, whether they have changed, and whether there is itching, pain or bleeding. Ask about other genital symptoms and take an appropriate sexual history, including recent and previous partners, sites of sexual contact, condom use, previous sexually transmitted infections (STIs) and testing. Pregnancy possibility matters because it affects treatment choices. Immune suppression is also relevant because warts may be more extensive or difficult to treat.

Examination is important because not every raised genital lesion is an HPV wart. Normal anatomical variants, molluscum contagiosum, condylomata lata associated with secondary syphilis, benign skin lesions and premalignant or malignant disease can resemble warts. Typical lesions are usually diagnosed visually. Bleeding, ulceration, induration, unusual pigmentation or another suspicious appearance should lower the threshold for biopsy, particularly where the diagnosis is uncertain. BASHH recommends urgent biopsy when malignancy is clinically suspected. (BASHH, 2024)

For the patient with high-risk HPV detected through cervical screening, the conversation is different. She may have no symptoms at all. Establish her previous screening history and explain what the current result actually shows. A cervical-screening result should not be used to decide when HPV was acquired or from whom. HPV may remain clinically silent for a long time, so a newly detected infection does not prove recent transmission or infidelity.

What investigations are recommended?

There is no routine blood test that tells someone whether they have genital HPV. Typical anogenital warts are generally a clinical diagnosis made by visual examination. Routine HPV typing of a wart is not required to diagnose it. Biopsy is used when the appearance is atypical, the diagnosis is uncertain or premalignant or malignant disease is suspected. (BASHH, 2024)

High-risk HPV testing has a different role within cervical screening. Screening arrangements vary across the four UK nations, so the programme should always be identified by nation rather than treating one schedule as universal UK practice.

In Scotland, women and anyone with a cervix aged 25 to 64 are routinely invited for cervical screening every five years. The cervical sample is tested for high-risk HPV first. If HPV is not detected, routine recall is usually in five years. If HPV is detected, cytology is used to look for cell changes. Depending on the result and whether HPV persists on subsequent testing, the person may return for earlier HPV testing or be referred for colposcopy, where the cervix is examined under magnification and biopsy can be taken if needed. (Public Health Scotland)

That distinction is useful for students: HPV testing identifies risk; cytology and colposcopy help identify whether abnormal epithelial change is present. Cervical intraepithelial neoplasia (CIN) describes precancerous cervical cell changes. CIN is not cervical cancer, and detecting and managing these changes is exactly how screening can prevent invasive disease.

How could HPV-related disease be managed?

There is no treatment given simply to eradicate an asymptomatic HPV infection. Management is directed at the disease HPV has produced and at surveillance of people at increased risk.

For anogenital warts, treatment removes visible lesions but does not guarantee immediate elimination of HPV from surrounding tissue, so recurrence can occur. BASHH treatment options include patient-applied therapies such as imiquimod and podophyllotoxin, and clinician-delivered approaches including cryotherapy, surgical excision, electrosurgery and other ablative treatments. There is no single best treatment for every patient. Lesion site and volume, pregnancy, immune status, previous treatment, local availability and patient preference all influence the choice. (BASHH, 2024)

Pregnancy changes some treatment choices, so medicines used for warts should not simply be continued or recommended without checking current guidance. Internal cervical, vaginal, urethral or anal lesions may also require specialist assessment because visualisation, differential diagnosis and treatment can be more complex.

For high-risk cervical HPV, management follows the cervical-screening pathway rather than wart treatment. Someone with HPV but no abnormal cytology may be recalled for repeat testing, while abnormal cytology or persistent HPV can lead to colposcopy and, where indicated, treatment of precancerous lesions.

Where does HPV vaccination fit?

Vaccination prevents infection with important HPV types before they have an opportunity to establish persistent infection. Scotland routinely offers HPV vaccination to all young people in S1, around 11 to 13 years of age. People who missed vaccination at school may still be eligible later, and eligibility should be checked against the current national programme rather than assuming previous sexual activity makes vaccination pointless. (NHS inform)

The population effect is already visible. Public Health Scotland reports that HPV vaccination protects against HPV-associated cancers and over 90% of genital-wart infections. Long-term Scottish data also show sustained protection against cervical disease, particularly when vaccination is given at age 12 to 13.

There is still work to do. HPV vaccination coverage among S1 pupils in Scotland was 72.6% in 2024/25, rising to 82.9% by S4, and uptake varied substantially by deprivation and geography. Vaccination is therefore not only an individual prevention intervention but also a public-health and health-inequality issue.

Vaccination does not replace cervical screening. Current vaccines protect against important oncogenic HPV types but not every type capable of causing cervical cancer, so eligible people should continue to attend screening when invited.

What should we explain to the patient?

For our first patient, begin with the fear she actually brought into the room. Typical genital warts are benign and are usually caused by low-risk HPV types. Having genital warts does not mean she has cancer, and it does not mean she will develop cervical cancer. Treatment can remove the visible lesions, although recurrence is possible.

For both patients, explain how common HPV is and how little a positive result can tell us about timing. HPV can be present without symptoms for long periods, so in most cases it is impossible to identify exactly when infection occurred or which partner transmitted it. This is particularly important when a patient interprets a new HPV result as evidence of infidelity.

For our second patient, explain that finding high-risk HPV does not mean cancer has been found. Her screening programme is designed to identify people whose cervix needs closer observation before cancer develops. If HPV is present but no cell changes are seen, follow-up testing allows the programme to see whether the infection clears or persists. If abnormal cells are identified, further assessment can take place before those changes become invasive disease.

Cervical screening can also be physically or emotionally difficult for some people, particularly following sexual trauma. In Scotland, patients can discuss adjustments such as a longer appointment, a smaller speculum, positioning changes or specialist support. Consent continues throughout the examination and the patient can ask for it to stop. (Public Health Scotland)

What could happen if HPV-related disease is not appropriately managed?

Untreated genital warts may persist, enlarge, multiply or recur, although some regress spontaneously. The main reason to reassess an atypical or changing lesion is not that an ordinary wart is expected to become cancer, but that another diagnosis or coexisting premalignant or malignant lesion may have been mistaken for a wart.

The more significant long-term concern is persistent high-risk HPV infection. Continued expression of oncogenic viral proteins can disrupt cell-cycle regulation and allow dysplasia to develop. Depending on anatomical site and HPV type, persistent infection contributes to cervical, anal, vulval, vaginal, penile and oropharyngeal cancers. Progression is generally measured over years and is not inevitable, which is precisely why vaccination and screening are so effective: vaccination prevents many infections from becoming established, while screening identifies risk and precancerous change before invasive cervical cancer develops.

In Scotland, cervical-screening coverage was 55.3% in 2024/25, below the programme's 80% target, with lower coverage in the most deprived areas. For nurses, encouraging informed participation in vaccination and screening is therefore part of prevention as well as patient education.

References

British Association for Sexual Health and HIV (BASHH) (2024) UK national guideline for the management of anogenital warts in adults. Available at: BASHH anogenital warts guideline.

NHS inform (2026) Cervical screening (smear test) in Scotland. Available at: NHS inform cervical screening.

NHS inform (2026) Who can get the HPV vaccine. Available at: NHS inform HPV vaccine.

Public Health Scotland (2025) High and low risk HPV. Available at: Public Health Scotland.

Public Health Scotland (2025) HPV immunisation statistics Scotland: school year 2024/2025. Available at: Public Health Scotland HPV immunisation statistics.

Public Health Scotland (2026) Scottish cervical screening programme statistics: annual update to 31 March 2025. Available at: Public Health Scotland cervical screening statistics.

Yim, E.K. and Park, J.S. (2005) ‘The role of HPV E6 and E7 oncoproteins in HPV-associated cervical carcinogenesis’, Cancer Research and Treatment, 37(6), pp. 319–324.