Human Papillomavirus and Genital Warts

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Synonyms: HPV, condylomata acuminata, condyloma acuminata, genital warts, penile warts, vulval warts, labial warts, anogenital warts, vaginal warts, cervical warts

Genital warts are a cutaneous manifestation of infection with the epidermotropic, sexually transmitted human papillomavirus (HPV). There are >100 of these double-stranded-DNA papovaviruses characterised, with most now fully DNA-sequenced.

  • HPV is transmitted sexually in most cases but can also be transmitted prenatally, by auto-inoculation or hetero-inoculation from non-genital warts and possibly by fomites.[2]
  • An individual's lifetime risk of HPV infection exceeds 50% but most are asymptomatically infected, with only about 1-2% developing genital warts.
  • About 90% of genital warts are caused by infection with HPV types 6 and 11. These types are not associated with a significant risk of neoplastic transformation.
  • Types 16 and 18 are associated with a high risk of neoplastic transformation.


Genital warts are the most commonly diagnosed sexually transmitted infection (STI) in the UK. One study in England, based on data from general practice and genitourinary medicine (GUM) clinics reported 80,531 new and 68,259 recurrent cases in the year 2008.[3]

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Risk factors[1][4]

  • Smoking.
  • Multiple sexual partners.
  • Early age of onset of sexual intercourse .
  • Illicit drug use.
  • Anoreceptive intercourse.
  • Manual sexual practices such as fisting and fingering increase the risk of anal warts.[5]
  • Immunosuppression (including iatrogenic variety in transplant recipients and HIV).[6]


The incubation period has been reported to be between three weeks to eight months. After this period, lesions may appear which are usually painless and asymptomatic but which may itch, burn, bleed or discharge. Urethral lesions may cause distortion of the urinary stream.

A relevant sexual history should be obtained to assess the risk of other STIs and sexual health needs:[8]

  • Other symptoms, eg urethral/vaginal discharge, pelvic or scrotal pain, intermenstrual or postcoital bleeding, dyspareunia.
  • Sexual activity in the preceding three 3 months.
  • Contraceptive and condom use.
  • Possibility of pregnancy.
  • HIV risk activities.


  • Lesions are usually papular and pink, red or brown and may be single but often multiple. A number of lesions may form a confluent mass. Over time the lesion may grow and develop into the classical florid warty appearance. They may become huge in immunocompromised patients.

  • Four types are seen:
    • Small papular.
    • Cauliflower floret.
    • Keratotic.
    • Flat-topped papules or plaques (usually seen on the cervix).
  • In males, genital warts mainly appear on the frenulum, corona, glans, prepuce, shaft and scrotum.
  • In females, they tend to be seen on the labia, clitoris, peri-urethral area and cervix.
  • Both sexes may be affected in the perineum, peri-anal area and anal canal.

The anogenital and surrounding skin should be examined under good illumination. Female patients should undergo a vaginal speculum examination, and proctoscopy may be indicated in both sexes if there is a history of anoreceptive sex. Recording lesions on genital maps can be useful to enable a visual record and monitor response to treatment.[9]

Diagnosis by biopsy and viral typing is not routinely required and tends to be reserved for where diagnosis is uncertain or for recalcitrant warts, warts with atypical features or where there is high risk of HPV-related malignancy.

  • Benign or malignant neoplasm (eg squamous cell carcinoma in situ, Bowen's disease).
  • Molluscum contagiosum.
  • Epidermoid cysts.
  • Hair follicles.
  • Sebaceous glands.
  • Pearly penile papules (normal variant: 1-3 rows of smooth, discrete, non-coalescing, 1-2 mm papules appearing on the margin of the glans).[11]
  • Hymen remnants.
  • Vulval papillomatosis (normal variant: regularly shaped, non-coalescing, largely symmetrical papillae on the inside of the labia minora and vestibule).[12]
  • Condyloma lata (secondary syphilis).

The majority of external genital warts are caused by HPV types 6 and 11 which are not associated with significantly increased risk of neoplastic transformation. However, 10% of genital warts are caused by HPV types 16 and 18 and these types are associated with an increased risk of:

  • Cervical carcinoma.
  • Vaginal, vulval and penile carcinoma.
  • Anal cancers.
  • Oral and oropharyngeal cancers.

General points:

  • Patients will require a detailed explanation of the condition with emphasis on long-term health implications for themselves and their partners. Reinforce with written information. Explain the long latent period associated with HPV and that recurrence of warts in one partner does not imply infidelity.
  • Data are conflicting regarding condom use. Current British guidelines suggest that condom use may be beneficial and advise their use, particularly in new relationships, although the evidence base for this is poor (see 'Prevention', below). Ideally, sexual contact with new partners should be avoided until the current warts have cleared. Individuals should be aware that the HPV persists after clinical clearance of warts for very variable lengths of time.
  • Psychological distress is common - referral for counselling may be appropriate.
  • 20-30% of patients with genital warts have concurrent STIs, so appropriate screening should be discussed and offered (including chlamydia, gonorrhoea, HIV, syphilis and hepatitis B and C).
  • Partner notification is not recommended.

Treatment of warts and screening for other STIs may occur within general practice or via the GUM clinic. Referral should occur where:[8]

  • The diagnosis is unclear.
  • There is suspicion of intra-epithelial neoplasia or malignancy (urgent referral).
  • There are internal warts in difficult-to-reach sites (intravaginal, cervical, urethral meatus or intra-anal).
  • The patient is a child, pregnant or immunosuppressed.
  • There is treatment failure or where treatment cannot be tolerated due to side-effects.
  • There are problematic recurrences.
  • There are positive results from the screen for other STIs.

There are many effective treatments, both topical and ablative and these tend to be selected largely on the preference of clinician and patient and the severity of disease.

The primary goal of treatment is to speed the clearance of symptomatic warts. Giving no treatment is also an option since warts regress spontaneously. Some evidence suggests that treatment may reduce HPV DNA persistence in genital tissues possibly reducing infectivity but there is no evidence that treatment reduces the incidence of cervical or genital cancer.

Only surgical treatments have clearance rates approaching 100%. The recurrence rate for new lesions occurring in previously treated or new areas is often in the region of 20-30% for all other therapies. All treatments are associated with itching, pain, burning and erosions.[14]

There is a lack of controlled trials comparing treatments, particularly in children and adolescents.[15]

Topical treatments[8][10][16]

For mild, early lesions, there is an emphasis on self-administered topical therapies such as podophyllotoxin and imiquimod which are effective and well tolerated and may be used for home treatment by patients (following a demonstration). However, where the number of warts is low, irrespective of type, ablative therapy from the outset is recommended.

  • Podophyllotoxin is suitable for soft, non-keratinised external genital warts. 0.15% cream should be used twice-daily for three days. If the wart persists, treatment may be repeated at weekly intervals, for a total of five weeks. Podophyllotoxin solution 0.5% is also available and may be used for warts which do not respond to the 0.15% cream. The solution is probably more convenient for penile warts whereas the cream is more useful for vulval and anal lesions.
  • Imiquimod is an alternative which can also be used for keratinised lesions. It should be applied thinly three times a week at night until the lesions resolve, for a maximum of 16 weeks.
  • Trichloracetic acid is less used due to its corrosive action on skin but is occasionally employed by hospital specialists for warts that are very indurated or in pregnant patients in whom other agents are contra-indicated.
  • All topical treatments can cause local skin reactions and, where severe, patients must stop treatment and seek advice. Normal surrounding skin may be protected from podophyllotoxin by the use of petroleum jelly. Avoid contact with broken skin and open wounds. Unprotected sexual contact soon after application should be avoided (as it may have an irritant effect on the partner). Condoms may be weakened if in contact with imiquimod.
  • Peri-anal warts are usually treated with imiquimod or cryotherapy. If persistent, they should be referred to the surgeons.
  • Cervical warts should be treated via colposcopy.
  • Other hospital-based treatments now available include carbon dioxide laser treatment and infrared coagulation.[1]
  • Treatments currently being evaluated include polyphenon E 10% cream (containing a mixture of green tea catechins)[17] and interferon injections.[1]
  • Warts in the urethral meatus are difficult to treat; refer to GUM or urology.

Care should also be taken in the treatment of pregnant patients. Avoid podophyllotoxin and imiquimod in pregnancy. Cryotherapy is often used to try to minimise lesions present at delivery but risks (perinatal transmission of genital warts, laryngeal papillomatosis, obstructed labour) to the baby are usually considered small and not an indication for Caesarean section.

Review should be undertaken at the end of a course of treatment. Change in treatment is indicated where a patient does not tolerate the current regimen or has under 50% response to current treatment by 6 weeks (8-12 weeks in the case of imiquimod).

Be suspicious of unusual presentations (eg flat or only slightly raised lesions, pigmented, indurated or ulcerated warts), particularly in patients aged over 35 years or with other risk factors, or of the development of new symptoms (eg itching, pain, crusting, bleeding) and warts that are unresponsive to treatment. Always arrange for biopsy to exclude malignancy.[18]

Genital warts in children

The discovery of external genital warts in children often raises concern about sexual abuse.[15] National Institute for Health and Clinical Excellence (NICE) guidance[19] recommends considering sexual abuse in a child younger than 13 years with anogenital warts unless there is clear evidence of:

  • Mother-to-child transmission during birth (it is not currently known at what age this can be confidently excluded).
  • Non-sexual transmission from a household member.

Studies suggest sexual transmission as the cause of infection in between 31-58% of children with anogenital warts. One study found an increase in HPV infection in children who had been abused.[20] However, it is often very difficult to determine the mode of transmission in children, even with viral typing of the index case and contacts, and the presence of warts or HPV infection without supporting social and clinical evidence cannot be taken as diagnostic of sexual abuse.[21] Advice should be sought from experienced child protection colleagues.[19]

Explain to patients that untreated external genital warts may:

  • Resolve spontaneously - up to one third spontaneously regress within three months.
  • Remain the same.
  • Increase in size.

Lifelong subclinical infection may persist. Warts may recur with or without immunosuppression, especially condylomata.

Patients should be reassured that over 90% of genital warts are caused by HPV types which are low-risk for neoplastic transformation.


Contrary to popular belief, condoms provide very little protection against skin-to-skin contact transmissible diseases such as HPV.[23][24]


A quadrivalent vaccine against HPV-6/11/16/18 (Gardasil®) has been developed to give protection against cancer of the cervix, precancerous lesions of the vulva and vagina and genital warts. It provides 96-100% efficacy at preventing genital warts when young women receive prophylactic vaccination and efficacy remains high for at least five years.[26] In Australia, where the quadrivalent vaccine has been part of their national immunisation strategy since 2007, a rapid and drastic reduction in the incidence of genital warts in women and men under the age of 21 has been reported.[27]

The UK Department of Health originally decided to back the bivalent vaccine against HPV-16 and 18 (Cervarix®) for the national HPV prevention programme. However, this decision has been reversed and Gardasil® has been recommended for use from September 2012.[28]

Studies suggest that the quadrivalent vaccine offers good protection against the development of genital warts in men and, in 2011, the American Advisory Committee on Immunization Practices (ACIP) recommended routine use of quadrivalent vaccine in males aged 11 or 12 years.[29] There are, however, no current plans to introduce a vaccine programme for males in the UK.

The current role of vaccination is solely prophylactic. Clinically active vaccines which can be used against HPV-related cancers are, however, in the process of development.[30]

Further reading & references

  • Condyloma Acuminatum, DermIS (Dermatology Information System)
  • No authors listed; Progress toward implementation of human papillomavirus vaccination--the Americas, MMWR Morb Mortal Wkly Rep. 2011 Oct 14;60(40):1382-4.
  • Woodhall SC, Jit M, Soldan K, et al; The impact of genital warts: loss of quality of life and cost of treatment in Sex Transm Infect. 2011 Oct;87(6):458-63. Epub 2011 Jun 2.
  • Arbyn M, Sanjose SD, Saraiya M, et al; EUROGIN 2011 roadmap on prevention and treatment of HPV-related disease. Int J Cancer. 2012 May 24. doi: 10.1002/ijc.27650.
  1. Rubano E et al, Genital Warts in Emergency Medicine, Medscape, Aug 2010
  2. Ghadishah D, Condyloma Acuminata, Medscape, Apr 2011
  3. Desai S, Wetten S, Woodhall SC, et al; Genital warts and cost of care in England. Sex Transm Infect. 2011 Oct;87(6):464-8. Epub 2011 Aug 3.
  4. Gearhart PA et al, Human Papillomavirus, Medscape, Jun 2012
  5. Jin F, Prestage GP, Kippax SC, et al; Risk factors for genital and anal warts in a prospective cohort of HIV-negative homosexual men: the HIM study. Sex Transm Dis. 2007 Jul;34(7):488-93.
  6. Ault KA; Epidemiology and natural history of human papillomavirus infections in the female genital tract. Infect Dis Obstet Gynecol. 2006;2006 Suppl:40470.
  7. Chuang T et al, Genital Warts, Medscape, Mar 2012
  8. Warts - anogenital, Prodigy (October 2008)
  9. Management of anogenital warts, British Association for Sexual Health and HIV (2007)
  10. Delaney EK, Baguley S; Genital warts. BMJ. 2008 Oct 17;337:a1171. doi: 10.1136/bmj.a1171.
  11. Korber A, Dissemond J; Pearly penile papules. CMAJ. 2009 Sep 15;181(6-7):397. Epub 2009 Aug 4.
  12. Wollina U, Verma S; Vulvar vestibular papillomatosis. Indian J Dermatol Venereol Leprol. 2010 May-Jun;76(3):270-2.
  13. Human papillomavirus (HPV) - cervical cancer and genital warts; Public Health England
  14. Lacey C et al, European Guideline for the Management of Anogenital Warts, International Union against Sexually Transmitted Infections (IUSTI), 2011
  15. Thornsberry L, English JC 3rd; Evidence-based treatment and prevention of external genital warts in female J Pediatr Adolesc Gynecol. 2012 Apr;25(2):150-4.
  16. British National Formulary; 63rd Edition (Mar 2012) British Medical Association and Royal Pharmaceutical Society of Great Britain, London
  17. Hoy SM; Polyphenon e 10% ointment: in immunocompetent adults with external genital and Am J Clin Dermatol. 2012 Aug 1;13(4):275-81. doi:
  18. Genital Warts, Sexually Transmitted Diseases Treatment Guidelines, Centers for Disease Control and Prevention (2010)
  19. When to suspect child maltreatment; NICE Clinical Guideline (July 2009)
  20. Unger ER, Fajman NN, Maloney EM, et al; Anogenital human papillomavirus in sexually abused and nonabused children: a Pediatrics. 2011 Sep;128(3):e658-65. Epub 2011 Aug 15.
  21. Jayasinghe Y, Garland SM; Genital warts in children: what do they mean? Arch Dis Child. 2006 Aug;91(8):696-700. Epub 2006 May 2.
  22. Juckett G, Hartman-Adams H; Human papillomavirus: clinical manifestations and prevention. Am Fam Physician. 2010 Nov 15;82(10):1209-13.
  23. Repp KK, Nielson CM, Fu R, et al; Male human papillomavirus prevalence and association with condom use in Brazil, J Infect Dis. 2012 Apr 15;205(8):1287-93. Epub 2012 Mar 6.
  24. Dediol I, Buljan M, Vurnek-A Ivkovia M, et al; Psychological burden of anogenital warts. J Eur Acad Dermatol Venereol. 2009 Sep;23(9):1035-8. Epub 2009 Mar 11.
  25. Human Papillomavirus (HPV) Vaccines, National Cancer Institute, 2011
  26. McCormack PL, Joura EA; Spotlight on quadrivalent human papillomavirus (types 6, 11, 16, 18) recombinant BioDrugs. 2011 Oct 1;25(5):339-43. doi: 10.2165/11205060-000000000-00000.
  27. Read TR, Hocking JS, Chen MY, et al; The near disappearance of genital warts in young women 4 years after commencing a Sex Transm Infect. 2011 Dec;87(7):544-7. Epub 2011 Oct 4.
  28. HPV vaccination; NHS Choices, 2012
  29. No authors listed; Recommendations on the use of quadrivalent human papillomavirus vaccine in MMWR Morb Mortal Wkly Rep. 2011 Dec 23;60(50):1705-8.
  30. van der Burg SH, Melief CJ; Therapeutic vaccination against human papilloma virus induced malignancies. Curr Opin Immunol. 2011 Apr;23(2):252-7. Epub 2011 Jan 13.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Chloe Borton
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Dr John Cox
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