Anogenital warts are small growths that appear on or around the genitals and anus, caused by certain types of the human papillomavirus. These warts are among the most common sexually transmitted infections, affecting hundreds of thousands of people each year, particularly young adults.
Epidemiology
Anogenital warts represent one of the most frequently encountered sexually transmitted infections worldwide. In the United States alone, an estimated 400,000 people receive a diagnosis of genital warts every year, with the majority being in their late teens and twenties. The condition is particularly common among teenagers and young adults who are beginning their sexual lives.[1][3]
The virus that causes these warts, known as human papillomavirus (a family of viruses that infect the skin and mucous membranes), is extraordinarily common. Approximately 79 million Americans have HPV at any given time. Nearly all sexually active people will become infected with at least one type of HPV at some point in their lives. Among those who contract the virus, at least 75% of sexually active adults have been infected with at least one type of anogenital HPV during their lifetime.[1][3][8]
Research has shown that anogenital warts may be more common in males than in females, though the condition affects both sexes substantially. The infection does not discriminate based on gender, and anyone who is sexually active can develop these warts. The demographic pattern shows a clear concentration among younger age groups, with most cases occurring between the ages of 15 and 30 years.[8]
An encouraging development has emerged in countries where HPV vaccination programs have been implemented. Among adolescents, young women, and heterosexual men in multiple countries including the United States, the incidence of anogenital warts has decreased following the widespread use of HPV vaccination. This represents a significant public health achievement in the prevention of this common infection.[2]
Causes
Anogenital warts are caused by infection with specific types of human papillomavirus. Among the more than 90 different HPV types that have been identified, types 6 and 11 are responsible for approximately 90% of all anogenital warts cases. These two particular strains are classified as low-risk or nononcogenic types, meaning they rarely lead to cancer.[2][3]
It is important to understand that HPV is a large family of related viruses, with more than 150 different types identified. At least 40 of these types can infect the anogenital area. While HPV types 6 and 11 cause visible warts, other types such as 16, 18, 31, 33, and 35 are occasionally found in anogenital warts as well, usually alongside types 6 or 11. These higher-risk types are associated with precancerous changes and can lead to various cancers, though the types causing visible warts themselves rarely cause cancer.[2][6]
The virus spreads primarily through direct skin-to-skin contact during sexual activity. When a person has sexual contact with someone who carries HPV, the virus can be transmitted even if no visible warts are present. The virus invades cells in the basal layer (the deepest layer of skin cells), penetrating through tiny breaks or abrasions in the genital skin and mucous membranes. After the virus enters these cells, there is typically a period of time before warts become visible.[6]
After HPV is transmitted, a latency period (time between infection and visible symptoms) can occur that ranges from 3 weeks to 9 months, or even longer in some cases. During this time, the virus is present but warts have not yet formed. Some people develop genital warts within weeks of sexual contact with an infected person, while for others it can take months or even years for warts to appear. This variability makes it very difficult to determine exactly when a person was infected or from whom they contracted the virus.[3][6]
The most common route of transmission is through sexual intercourse, including vaginal, anal, and oral sex. However, the virus can also spread through genital touching or skin-to-skin contact without penetration or ejaculation. A person can transmit HPV to their partner through oral sex, either by giving oral sex to someone who has HPV or genital warts, or by receiving oral sex from someone who has HPV or warts on their mouth, lips, or tongue. The virus prefers genital areas over the mouth, but oral transmission is possible.[3][8]
In addition to sexual transmission, there are other less common routes. Vertical transmission can occur from mother to baby during childbirth as the infant passes through the birth canal. This can potentially lead to warts in the infant’s respiratory tract, though this is rare. Anogenital warts can also affect infants and young children through transmission during birth or from the hands of caregivers. Auto-inoculation, where a person transfers the virus from one part of their body to another, is another possible route.[8]
Risk Factors
Several factors can increase a person’s risk of developing anogenital warts. The most significant risk factor is being sexually active without using protective barriers. People who do not use condoms or dental dams during sexual activity have a higher chance of contracting HPV and developing genital warts. While condoms can reduce the risk, they do not provide complete protection because they do not cover all genital skin areas where HPV can be transmitted.[3]
Having multiple sexual partners substantially increases the risk of getting genital warts. Each new sexual partner represents a potential exposure to HPV. The virus is so common that the more partners a person has, the more likely they are to encounter someone who carries HPV. Conversely, being in a mutually monogamous relationship with one partner who only has sex with you can reduce this risk.[3]
Age is another important risk factor, with anogenital warts being most common in people between 15 and 30 years of age. This pattern reflects both behavioral factors, as younger people may be more likely to have multiple partners or new partners, and immunological factors related to first exposures to the virus.[8]
Immunocompromised individuals face a particularly high risk of acquiring HPV and developing anogenital warts. People who have weakened immune systems due to drug-induced immunosuppression, such as those taking medications after organ transplants, or those with HIV infection, are more vulnerable to HPV infection. Their immune systems are less able to fight off the virus or control its replication, which can lead to more extensive and persistent warts.[8]
Smoking tobacco appears to increase the risk of developing genital warts. Research indicates that smokers are at higher risk compared to non-smokers. Additionally, warts are more likely to return after treatment in people who smoke. The mechanisms behind this association are not completely understood but may involve the immune-suppressing effects of tobacco smoke.[3]
Having unprotected sex with someone who has genital warts dramatically increases transmission risk. About two out of every three people who have sexual contact with someone infected with genital warts will catch the virus. The warts usually appear within three months of contact, though the timeframe can vary considerably. Transmission is more likely from visible warts than from subclinical or latent HPV infection, meaning the risk is highest when warts are actually present and visible.[8][9]
Women who are pregnant may find that existing genital warts enlarge and multiply during pregnancy. Hormonal changes and alterations in immune function during pregnancy can affect how the body responds to HPV, potentially causing warts to grow larger or become more numerous.[8]
Symptoms
Anogenital warts typically appear as small, flesh-colored bumps or growths on the skin in the genital and anal regions. The appearance of these warts can vary considerably from person to person. They may be small or large, raised or flat, and can appear individually or in groups. When warts cluster together, they often take on a distinctive bumpy, cauliflower-like appearance. Some warts are very tiny and may go unnoticed, while others can grow to several centimeters in size.[1][3]
The warts can form in numerous locations throughout the anogenital area. In women, they commonly appear on the vulva, the walls of the vagina, the cervix, and the area between the outer genitals and the anus. In men, warts frequently develop on the tip or shaft of the penis, on the scrotum, and around the anus. Common sites include around the vaginal opening, under the foreskin of uncircumcised men, and on the shaft of the penis in circumcised men. Warts can also occur inside the anal canal, vagina, urethra, or on the perineum. Internal warts affecting the cervix, vagina, urethra, or anus may not be visible without medical examination.[1][2]
In most cases, anogenital warts are asymptomatic, meaning they do not cause any physical discomfort or symptoms beyond their appearance. However, depending on their size and location, they can sometimes cause various symptoms. Some people experience itching or irritation in the affected area. Discomfort or mild pain can occur, particularly if warts are in locations subject to friction during movement or sexual activity.[2][3]
Bleeding can occur with genital warts, either spontaneously or during sexual intercourse. This happens because warts can be fragile and may bleed easily if they are bumped, rubbed, or otherwise traumatized. Some people experience pain or discomfort during sex if warts are present. Women may notice bleeding between periods or after intercourse if warts are located on or near the cervix.[1][3]
Changes in urination can occur if warts are located near or in the urethra. Problems with urination may include difficulty starting the stream, stopping and starting frequently, changes in the direction of urine flow, or even blood in the urine. Warts that grow large enough can potentially obstruct the flow of urine or, in rare cases, interfere with bowel movements if they are located around the anus.[5]
The physical appearance of warts can vary in color and texture. Most are flesh-colored or skin-colored, but they can also appear white, red, pink, or darker than the surrounding skin. They typically feel soft to the touch, though some may be firmer. The texture is often described as rough, similar to tiny bumps on the skin’s surface. A wart may have a folded or irregular surface, especially when multiple warts grow close together.[3][5][8]
Some warts are flat and may be less noticeable than raised warts. Others can take on a stalk-like or pedunculated (attached by a narrow stalk) appearance. If the virus has been introduced along a scratch or small tear in the skin, warts may appear in a linear pattern following that injury.[2][8]
Importantly, many people who are infected with the types of HPV that cause genital warts never develop any visible warts at all. They may have no symptoms whatsoever and may not even know they have been infected. Despite having no visible warts, these individuals can still transmit the virus to sexual partners. This is why genital warts and HPV infection are so common and why they spread so readily through populations.[7][9]
Prevention
The most effective way to prevent anogenital warts is through HPV vaccination. Vaccines are available that protect against the HPV types that cause most cases of genital warts. These vaccines are most effective when given before a person becomes sexually active and is exposed to HPV. The vaccine is typically recommended for children and young adults, usually starting around age 11 or 12, though it can be given as early as age 9. People up to age 26 who have not been vaccinated should talk to their doctor about receiving the vaccine. The vaccination requires a series of shots, typically given over several months, and provides the best protection when all doses are completed before first sexual contact.[1][7]
Using barrier protection during sexual activity can significantly reduce the risk of contracting or spreading genital warts. Latex condoms, when used correctly and consistently during every sexual encounter, can lower the chances of HPV transmission. However, it is important to understand that condoms do not provide complete protection. HPV can infect areas of genital skin that are not covered by a condom, so transmission can still occur even with consistent condom use. Despite this limitation, condoms remain an important tool for reducing risk.[7][9]
Dental dams should be used during oral sex to reduce transmission risk. These thin barriers can be placed over the vulva or anus during oral contact. For people engaging in any form of sexual activity, using these protective barriers consistently is an important prevention strategy.[7]
Limiting the number of sexual partners can reduce the risk of exposure to HPV. Being in a mutually monogamous relationship, where both partners only have sex with each other, lowers the chance of encountering HPV. Each new sexual partner represents a potential exposure to the virus. The only certain way to completely avoid HPV is to abstain from all forms of sexual contact, including oral, vaginal, and anal sex. However, most people choose to be sexually active at some point, so understanding risk reduction is important.[7]
If you notice warts on a sexual partner’s genitals or anus, avoid sexual contact with that person until they have been evaluated and treated. The risk of transmission is highest when visible warts are present, though transmission can occur even when no warts are visible. Open communication with sexual partners about sexual health is an important prevention strategy.[7]
Avoiding or quitting smoking can help prevent genital warts and reduce the likelihood of recurrence after treatment. Research has shown that smokers have a higher risk of developing warts compared to non-smokers, and warts are more likely to return after treatment in people who smoke. Quitting smoking supports overall immune function and may help the body control HPV infection more effectively.[3]
For women, regular cervical screening (Pap tests) is important for detecting abnormal changes caused by HPV, though these tests do not prevent genital warts specifically. Women aged 21 to 65 should follow recommended screening schedules. While cervical screening does not detect genital warts, it is crucial for identifying precancerous changes that high-risk HPV types can cause.[7]
Getting tested for sexually transmitted infections regularly is part of maintaining sexual health. While there is no routine screening test specifically for genital warts or HPV in most circumstances, regular checkups allow for early detection and treatment. If genital warts are diagnosed, informing sexual partners so they can be evaluated is important for preventing further spread.[3]
Pathophysiology
The development of anogenital warts involves a complex process that begins when human papillomavirus penetrates the skin or mucous membranes in the genital area. The virus gains entry through microscopic breaks, abrasions, or areas of minor trauma in the epithelial surface. These tiny openings in the skin barrier allow the virus to reach the deeper layers where it can establish infection.[6]
Once the virus enters the body, it specifically targets and invades cells in the basal layer of the epidermis. The basal layer is the deepest part of the epidermis where new skin cells are constantly being produced. HPV has a particular affinity for these actively dividing cells. The virus infects keratinocytes (the primary type of cell found in the epidermis) in the skin and epithelial cells (cells that line mucous membranes) in mucosa, stimulating them to multiply abnormally.[6][8]
After initial infection, the virus typically enters a latency period that can last anywhere from 3 weeks to 9 months, or sometimes even longer. During this latent phase, the virus is present in the cells but may not be actively producing visible changes. The infected cells harbor viral DNA, but warts have not yet formed. This latency explains why there can be such a long delay between when a person is exposed to HPV and when warts finally appear.[6]
Following the latency period, if the immune system does not successfully clear the infection, the virus begins active replication. Viral DNA directs the production of viral proteins and new virus particles. The virus causes infected keratinocytes to proliferate excessively, leading to a thickening and overgrowth of the epithelium. This abnormal proliferation of cells is what creates the visible wart structure that projects above the normal skin surface.[6]
Infected cells undergo characteristic morphological changes. One of the hallmark features visible under microscopic examination is koilocytosis (abnormal cell changes characterized by enlarged cells with irregular, darkened nuclei surrounded by a clear halo). These koilocytic cells are a distinctive sign of HPV infection and help pathologists confirm the diagnosis when tissue samples are examined under a microscope.[6]
The specific sites most frequently affected by anogenital warts reflect areas where the virus can most easily gain entry and where the right type of epithelium exists to support viral replication. Common sites include the penis, vulva, vagina, cervix, perineum, and perianal area. The virus shows preference for warm, moist areas of skin and mucous membranes. Occasionally, warts can also form in the oropharynx, larynx, or other mucosal surfaces if the virus is transmitted through oral contact.[6]
HPV types 6 and 11, which cause most genital warts, are classified as low-risk types because they do not typically cause cancer. These viral types have low or absent oncogenic potential (ability to cause cancer). However, other HPV types such as 16, 18, 31, 33, and 35 are occasionally found in anogenital warts, usually alongside types 6 or 11. These high-risk types can be associated with areas of abnormal cell growth that may progress to precancerous changes, particularly in people who have weakened immune systems such as those with HIV infection.[2][4]
The body’s immune response plays a critical role in controlling HPV infection. In most cases, the immune system recognizes and eliminates HPV infection within months to a couple of years without any treatment. About 9 out of 10 HPV infections resolve on their own within two years as the immune system clears the virus. This is why some genital warts disappear spontaneously without any medical intervention. However, in some individuals, particularly those with weakened immune systems, the infection persists and warts continue to grow or recur even after treatment.[7]
The natural history of anogenital warts varies considerably. If left untreated, warts may resolve spontaneously, remain unchanged in size and number, or increase in size and number. Complete resolution of lesions after 2 years occurs in approximately 75% of individuals without any intervention. However, for many people, the cosmetic concerns, discomfort, or psychological distress associated with visible warts prompts them to seek treatment rather than wait for spontaneous resolution.[15]
Even after visible warts are treated and removed, the underlying HPV infection may persist in surrounding normal-appearing tissue. This is why warts can recur even after apparently successful treatment. The virus may remain in a latent state in nearby cells and can be reactivated later, leading to new wart formation. This persistent infection also means that a person who has had genital warts treated can still transmit HPV to sexual partners, even when no visible warts are present.[2]