Genital warts in females There have been studies, however, that have detected HPV DNA in cervical or vulva-vaginal samples from women who have not had sexual intercourse8. Transmission of HPV is enhanced when the superficial epithelium is disrupted6, as this is where the infectious agent resides4. The HPV life cycle begins with infection of the basal cell layer of the epithelium and progresses with epithelial cell differentiation, resulting in complete virions present in the epithelial cells in the superficial layer4. The greatest risk of transmission is likely to exist when genital warts are present, as they reflect a productive HPV infection. The risk of transmission of HPV to offspring is also a concern. The increasing frequency of child- hood genital warts has been proposed to be the result of sexual abuse5. However, an association between genital warts and cutaneous HPV 223 has also been reported. There may also be a non-sexual transmission of genital warts from mothers, as well as the possibility of transmission during passage through the birth canal if mothers have external or cervical genital warts5. Additional data support a vertical (transplacental) transmission of HPV DNA, as over 50% of children born to HPV 16- or 18-infected mothers were positive for these HPVs24. PSYCHOLOGICAL ASPECTS OF GENITAL WARTS Genital warts are not only cosmetically unaccept- able and associated with discomfort and pain, but they are also associated with emotional stress25. It is reported that the psychological stress of having genital warts is often greater than the medical effects of the disease26. Some of the psychological outcomes of patients with genital HPV infection are impairments to their sex life, a fear of cancer and a worsening of the emotional relationship with their partner27. In an international survey of patients’ percep- tions about genital warts it was found that 61% of women were ‘quite’ or ‘very’ concerned about having genital warts25, with recurrence and trans- mission being of the greatest concern. In total, 95% of women believed that there was a risk asso- ciated with genital warts; the most commonly mentioned risks were a link to cervical cancer or to Gall an unspecified cancer. In terms of lifestyle, approx- imately 40% of women said that having genital warts had changed their lifestyle. Sexual behavior had particularly changed, resulting in an increase in condom usage during sexual intercourse, absti- nence from sexual intercourse, increased caution about new partners and a decrease in the number of sexual partners25. TREATMENT OF GENITAL WARTS Treatment of genital warts can be a frustrating experience for both physician and patients28. There are many current treatments for genital warts; however, none are successful in all three goals of therapy: complete eradication of warts, maintaining clearance and eliminating the virus. Recurrence is a substantial problem, as many therapies do not eradicate the reservoir of HPV DNA that is present in the tissue located adjacent to the genital wart. Current therapies are composed of both abla- tive and cytodestructive modalities. Physically ablative therapies include cryotherapy, laser therapy, electrosurgery and surgical excision. Many of the physically ablative therapies have high initial success rates; however, recurrence rates are also high28. Cytotoxic agents that treat genital warts destroy the affected tissue either by chemo- destructive or antiproliferative modes of action. Cytotoxic agents include podophyllin, podofilox (podophyllotoxin), trichloroacetic acid (TCA) and 5-fluorouracil. Eradication of genital warts by stimulation of the immune system is an alternative strategy for genital wart therapies. Interferon, an antiviral, immunomodulatory agent is effective in treating genital warts when administered intralesionally2, and can be used as a treatment for recalcitrant warts. Imiquimod is an immune response modifier that acts to induce both humoral (innate) and cellular immunity. The antiviral and antitumor activity of imiquimod is believed to be the result of the induction of cytokines such as interferon-a, tumor necrosis factor-a and a number of specific interleukins29. It is this stimulation of the immune system to fight the HPV infection that is the pro- posed mechanism for eradication of genital warts by imiquimod. INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY 151