Causes and spread of genital warts

　　Human papillomavirus is infected through unclean sexual intercourse or indirect contact. After the virus infects the human body, it lurks between the basal horn prion cells of the external genitalia. The incubation period is generally 1-6 months, with an average of 3 months. Later, as the epidermal cell layer replicates, the human papilloma virus invades the cell nucleus, causing cells to divide rapidly. At the same time, accompanied by the reproduction and dissemination of virus particles, characteristic papillomas are formed, which appear as vegetations of different shapes and sizes. The pathogen of genital warts is human papillomavirus. The main source of infection is patients with genital warts. The main transmission routes are as follows:

　　(1) Direct sexual contact infection: This is the main route of transmission. When having sexual intercourse with a patient suffering from genital warts, the warts growing on the external genitalia are exophytic and brittle, so the surface is easily scratched, and the viruses in the warts and epidermal tissue are shed. Vaccination On the genitals of sexual partners, causing human papilloma virus infection. Therefore, genital warts are easy to occur in people with chaotic sexual relationships.

　　(2) Mother-to-child transmission: Pregnant women with genital warts, especially clinical Symptoms are not obvious but Uterus Pregnant women with viral infection in the neck will have viruses in their reproductive tract. During delivery, fetus After passing through the birth canal, it causes viral infection in newborns and causes genital warts in infants and young children.

　　(3)Indirect transmission: Some patients with genital warts are infected with human papillomavirus through indirect means, most commonly through daily necessities such as underwear, bath towels, bathtubs, etc. Therefore, outbound travelers and tourists should pay great attention to this approach.

　　Pathogenesis

　　HPV infection of genital warts is transmitted through sexual contact. Small trauma at the contact site can promote infection. Three types of squamous epithelium ( skin , mucosa, metaplasia) are sensitive to HPV infection. Each type of HPV is associated with specific clinical damage and has its own predilection sites on the skin or mucosal squamous epithelium. Infection may occur when exfoliated surface cells or keratin fragments containing a relatively large number of viral particles enter the cracks of susceptible epithelium. It can be caused by direct contact or rarely by automatic inoculation or contaminated underwear, bathtubs, bath towels, and bedpans.

　　After the virus infects the human body, it can lurk between basal keratinocytes and replicate in the epidermal cell layer. HPV invades the cell nucleus and causes rapid cell division. At the same time, it is accompanied by the reproduction and dissemination of viral particles, forming characteristic papilloma. Late genes express structural polypeptides, that is, structural protein assembly particles appear. The virus is mainly concentrated in the nucleus in the granular layer. An increase in hollow cells appears in the granular layer of the epidermis. Histologically normal epithelial cells also have HPV. Residual DNA after treatment can often cause disease of recurrence.

　　HPV causes warts on the skin and proliferation on the pharynx, perianal, and genital mucous membranes sexually transmitted diseases The virus type is a small DNA virus. Most of the lesions caused by HPV infection are benign and can resolve on their own, but there are also cases of worsening. For example, there are reports of squamous cell carcinoma forming on the perianal and genital mucosa. There are also rare hereditary skin diseases, skin cancer secondary to epidermodysplasia verruciformis (EV), etc., in which HPV has been detected in cancer cells.