Self-reported incidences of clinically diagnosed genital warts confirm that these are common in both women and men. Ever having had clinically diagnosed genital warts was reported by 10.6% of almost 70,000 Nordic women aged 18 to 45 years in 2005 and by 7.9% of almost 23,000 Danish find more men in the same age category in 2007 [9] and [10]. In 2000, in the UK, 4.1% of women and 3.6% of men aged 16–44 years reported ever being diagnosed with genital warts [11].
In the United States (1999–2004, age category 18–59) and Australia (2001–2002, age category 16–59), the cumulative incidence was 7.2% and 4.4% among women, respectively, and 4.0% among men [12] and [13]. Human papillomaviruses are small non-enveloped DNA DAPT nmr viruses that belong to the Papovaviridae family. The viral capsid is composed of two proteins: the major L1 and minor L2 proteins. There are 170 different HPV types identified, 40 of which infect the genital tract [14]. These mucosal HPV types
are classified as low-risk (LR) and high-risk (HR) types based on the prevalence ratio in cervical cancer and its precursors. LR-HPV types, such as 6 and 11, induce benign lesions with minimal risk of progression to malignancy, HR-HPV have higher oncogenic potential. Approximately 99% of cervical cancers contain HPV DNA of HR-HPV types, with type HPV16 being the most prevalent, followed by types 18, 31, 33, and 45 [15]. Most HPV infections are transient and are spontaneously cleared or suppressed by the host immune response. It is unclear whether these infections resolve by complete viral clearance or by maintenance of a latent phase in the basal cells of the epithelium, in which the virus replicates at extreme low levels without full viral expression [16]. Infections that are not cleared at an early 4-Aminobutyrate aminotransferase stage progress towards premalignant squamous intraepithelial lesions (SIL), histopathologically referred to as cervical intraepithelial neoplasia (CIN). Low-grade lesions, LSIL (cytological classification) or CIN1 (histological classification), represent a chronic HPV infection in which HPV DNA is episomal and intact virion production
and shedding occurs (both by high-risk HPV as well as low-risk HPV, e.g. HPV11). Lesions are frequently cleared by the immune system, however, some lesions do not spontaneously regress and can persist for a long period. Viral persistence within the host cells is an uncommon event that is necessary for progression to malignancy. Clonal progression of the persistently infected epithelium can lead to high-grade lesions (HSIL or CIN2-3), which in turn can progress towards invasive disease [16]. The progression towards high-grade disease (HSIL/CIN3) is often with a different strain of HPV and not necessarily a progression of low-grade disease. HIV infected women have a higher prevalence of HPV infection and are often infected with multiple HPV types.