Human papillomavirus (HPV) infection !
Human papillomavirus (HPV) infection is very common and sexually spread; most infections clear on their own, but some types cause warts or cervical cancer.
Updated 2026-10-30
Structures involved
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In biochemistry
Microorganisms that cause it
In histology
- Cell cycle, mitosis and meiosis
- Cell adaptations: hypertrophy, hyperplasia, atrophy, metaplasia
- Cervix and vagina: the transformation zone
Why it happens
- Oncogenic viruses and H. pylori: the table to know
- Dysplasia and carcinoma in situ
- Cytology: the Pap test, fine-needle aspiration and body fluids
- Oncogenes and tumour suppressor genes
What it is
Infection with human papillomavirus, a DNA virus passed mainly by sexual skin-to-skin contact. Most infections clear on their own; low-risk types cause genital warts and persistent high-risk types can cause cervical and other anogenital and oropharyngeal cancers.
Who gets it
The most common sexually transmitted infection worldwide; most sexually active women and men acquire it at some point. In HPV-positive Latin American women from the ESTAMPA screening study, HPV16 was found in 65.1% of cervical cancers. In Colombia, HPV vaccination for girls is part of the national programme, and organised cervical screening exists.
Causes
- Human papillomavirus, with many types
- Low-risk types (mainly 6 and 11) cause anogenital warts
- High-risk types (mainly 16 and 18, plus others) cause precancer and cancer
- Spread by genital, anal or oral skin and mucosal contact; also from mother to newborn (rare)
Risk factors
- Early sexual debut
- Multiple sexual partners or a partner with multiple partners
- Immunosuppression, including HIV infection
- Smoking (increases persistence and progression to cervical cancer)
- No vaccination
Pathophysiology
The virus reaches basal epithelial cells through microabrasions, especially in the cervical transformation zone. Most infections are cleared by the immune system. In persistent high-risk infection, viral proteins E6 and E7 inactivate p53 and Rb, allowing uncontrolled proliferation, precancerous lesions and, over years, invasive cancer.
Classification
- Low-risk types: anogenital warts (condylomata acuminata), recurrent respiratory papillomatosis
- High-risk types: low- and high-grade squamous intraepithelial lesions (CIN 1–3) and cancer
- Sites: cervix, vagina, vulva, anus, penis and oropharynx
Symptoms and signs
- Usually no symptoms
- Anogenital warts: soft, flesh-coloured, cauliflower-like papules on the vulva, perineum, vagina, cervix or perianal skin
- Itching or discomfort from warts
- Precancerous lesions cause no symptoms and are found by screening
Diagnosis
- Clinical
- Genital warts are diagnosed by their appearance. Precancerous lesions are detected through cervical screening and confirmed by colposcopy and biopsy.
- Tests
- Cervical cytology (Papanicolaou) and high-risk HPV testing for screening; visual inspection with acetic acid is used in some settings; biopsy of atypical lesions; tests for HIV, syphilis and other sexually transmitted infections.
- Imaging
- Not needed for infection; colposcopy (a magnified examination) guides biopsy of the cervix.
Differential diagnosis
- Molluscum contagiosum
- Condylomata lata of secondary syphilis
- Vestibular papillomatosis (normal variant)
- Seborrhoeic keratosis or skin tags
- Vulvar intraepithelial neoplasia or carcinoma
Goal of treatment
There is no antiviral cure: treatment removes warts and precancerous lesions, prevents progression to cancer and reduces transmission.
Treatment
- Medical
- Topical patient-applied or clinician-applied treatments for warts: immune response modifiers or cytotoxic agents.
- Procedure
- Cryotherapy, excision, electrocautery or laser for warts.
- Procedure
- Treatment of cervical precancer by ablation (cryotherapy or thermal ablation) or excision (loop electrosurgical excision or conisation).
- Follow-up
- Follow-up with cytology and HPV testing after treatment, according to national guidelines.
Drugs for this condition
Complications
- Cervical, vaginal, vulvar, anal, penile and oropharyngeal cancer
- Recurrent warts
- Recurrent respiratory papillomatosis in children after perinatal transmission
- Psychological distress
Prognosis
Most infections clear within one to two years. Warts often recur but are benign. Precancerous lesions found through screening are highly curable.
Prevention
- HPV vaccination, most effective before sexual debut
- Regular cervical screening according to national guidelines
- Condoms reduce but do not eliminate transmission
- Not smoking
Test yourself
Think of the answer, then tap the question to see it.
Which HPV types cause most genital warts?
Low-risk types 6 and 11.
Which HPV types cause most cervical cancers?
High-risk types 16 and 18.
How do HPV proteins E6 and E7 promote cancer?
E6 leads to degradation of p53 and E7 inactivates the retinoblastoma protein (Rb), removing cell-cycle control.
In which part of the cervix do HPV-related lesions usually arise?
In the transformation zone, where columnar epithelium changes to squamous epithelium.
When is the HPV vaccine most effective?
When given before sexual debut, before exposure to the virus.
Related conditions
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Human Papillomavirus (StatPearls (NCBI Bookshelf), 2023); Distribution of human papillomavirus genotypes by severity of cervical lesions in HPV screened positive women from the ESTAMPA study in Latin America (PloS one, 2022) · adapted, CC BY 4.0.
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