Aetiology

Genital warts are caused by infection with human papillomavirus (HPV), a non-enveloped, double-stranded DNA virus.[13] Productive infection and subsequent hyperproliferation occur once the virus has entered basal epithelial cells.[7]​​[14]

More than 150 HPV types have been identified, including approximately 40 types that infect the genital area.[15][16] These types are further divided into low-risk types (6, 11, 42, 43, 44) and high-risk types (16, 18, 31, 33, 35, 39, 45, 52, 55, 56, 58).​[6]​[7]​​​​ The distinction between high- and low-risk types is based on the associated risk of anogenital carcinoma development.[13] Genital warts are most commonly caused by HPV types 6 and 11, which have low potential for oncogenesis.[8][13][17][18]

Pathophysiology

Infection with human papillomavirus (HPV) occurs most commonly through direct contact with individuals with clinical or subclinical HPV lesions.[13] Infection can also occur from contact with contaminated surfaces or objects. Auto-inoculation from one site to another is also common among people with genital warts.[5] The primary targets for HPV infection are basal keratinocytes. Under normal conditions, the virus cannot gain entry into these cells due to overlying differentiated cell layers, which create a mechanical barrier. It is thought that a form of trauma such as an abrasion or microdefects through maceration of the area is required to disrupt this barrier, thus allowing virus entry.[19]

Upon entry, the virus undergoes a variable latency or pseudolatency period, referring to low-level DNA replication.[1] A clinically apparent lesion eventually develops after viral-induced basal cell proliferation occurs. Viral DNA replication and mature virion assembly is amplified as the virus migrates up the epidermal strata within differentiating keratinocytes.​[7]​[17]

Cell-mediated responses are primarily responsible for controlling HPV infection. In immunocompetent patients, most genital HPV infections are spontaneously cleared by the host immune defence mechanisms.[17] It is estimated that 10% to 30% of genital warts resolve in 3 months of onset without treatment.[7]​ Evidence of the importance of this mechanism is supported by an increased prevalence of warts in patients with cell-mediated immune deficiencies, such as HIV infection. Patients with humoral immune deficiencies are not similarly affected. In addition, a lower rate of spontaneous regression of genital warts is seen in cell-mediated deficiencies, with an increased rate of recurrences.[20]

Classification

Clinical location​[7]​

  • Genital: involvement of the glans penis, prepuce, shaft, or scrotum in males, and the labia, clitoris, vagina, or cervix in females.

  • Anal: involvement of the anal canal, or perianal or rectal areas.

  • Anogenital: involvement of both areas listed above.

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