During the middle of the 20th century, genital warts were found to be caused by the human papilloma virus (HPV), of which there are more than 100 genotypes. Genital warts, like skin warts and verrucas, are epidermal tumours; while some genotypes are more related to wart development than others (e.g. types 6 and 11), some are more associated with cervical intraepithelial neoplasia and carcinoma of the cervix (e.g. types 16 and 18)1
Many people with HPV infection do not have genital warts. Initially, the wart formation process is via a port of entry in traumatised skin epithelium, into the basal germinal layer. The virus then multiplies inside the nuclei of the basal cells, which are the only dividing cells in the skin epithelium, resulting in the warty appearance of hyperkeratosis, hyperplasia, or overgrowth of the horny layers.
The most usual route of infection is via sexual contact; however, perinatal transmission and, occasionally, transmission from hand warts in children have also been attributed to the transfer. There is no evidence that they are caused by fomites.
Factors other than sexual activity have been associated with a risk of acquiring genital warts. Smoking cigarettes and the use of ultraviolet sunbed radiation both decrease the Langerhans cell-mediated immune response and suppress natural killer cell activity.2