Keywords: genital warts etiology and pathology

    Etiology

    HPV cause warts on the skin, the formation of proliferative lesions in the pharynx, perianal and genital mucosa, the virus type of small DNA viruses. Infected with HPV lesions occur most are benign and can be self-limiting but also deteriorate cases. Perianal and genital mucosa formed on the reports of squamous cell carcinoma. There are rare genetic skin diseases, warts like epidermal dysplasia (EV), the renewal skin cancer, HPV detection in cancer cells.

    HPV papovavirus Branch A is a member of the virus particle diameter of 50-55nm film constitute 20 icosahedral capsid, the cyclic double-stranded DNA having a 7900 base pair composition, the size of the electron microscope of virus particles, morphology polyomavirus and mouth are very similar. Papillomavirus (PV) has a species-specific HPV have not been able to multiply in tissue culture or in experimental animal models.

    The virus structural proteins: 85% of PV particles, the major capsid protein by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS – PAGE) to determine if the virus has a molecular weight of 56.000; minor capsid protein, molecular weight migration in 76.000, found four cell histone viral DNA.

    Similar to the structure of the viral genome of all HPV can be determined in accordance with the procedures for DNA hybridizing under stringent conditions, the type and subtype of the virus, a different type of HPV DNA and other types of viral DNA occurs only 50% of cross-hybridization, and so far has been found that more than 60 kinds of HPV types, with in-depth research, you will be identified more HPV types.

    Pathogenesis

    Of genital warts HPV infection transmitted through sexual contact, the contact area of ​​trauma can promote infection, three types of squamous epithelium (skin, mucous membranes, chemical and biological weapons) against HPV infections are sensitive. Each HPV type special clinical damage of the skin or mucosal squamous own predilection sites. Shedding of superficial cells contain a relatively large number of virus particles or keratin debris into the susceptible epithelial fractures, infection may occur, it may be due to direct contact or rare auto-inoculation or contamination underwear, bidet, bath towels, potty infection.

    Human infection can lie dormant in the basal keratinocytes, epidermal cell layer replication, HPV invasive nucleus, causing the cells to rapidly dividing, accompanied by the propagation and spread of the virus particles, the formation of the characteristic of papillomas. Late gene expression structure of polypeptides that appear to structural proteins assembled particles, the virus mainly concentrated in the particle layer of the nucleus, in the epidermis particles layer appears koilocytotisis increased histologically normal epithelial cells also have of HPV DNA after treatment residue of can often lead to recurrence of the disease.

    The host response to HPV infection caused by the immune response, including the two aspects of cellular immunity and humoral immunity.

    First, the cellular immune

    One of the important foundation of human cells immune status affect CA outcome. Cellular immunity is more important than the humoral immune. Clinical genital warts associated with cellular immune defects in patients with rash often persistent, an increase in the number of suppressor T cells in the peripheral blood NK cell dysfunction, r-interferon and interleukin-2 production was reduced and dissipated wart lesions often infiltration of activated T cells and NK cells, some of keratinocyte HLA-DR positive.

    Immune suppression or immune deficiency increased the incidence of genital HPV infection and HPV-related diseases. Genital warts in depletion of helper T cells, CD4/CD8 ratio inversion, and its value is <1. In the the CA patient’s peripheral blood suppressor / cytotoxic T cells was significantly higher ratio of helper / inducer T cells and Auxiliary / suppressor T cells was reduced. CA cervix and cervical intraepithelial tumor-like lesions (CIN) lesions Langerhans cells decreased significantly. CA of NK cells to produce the r-interferon and interleukin-2 reduced. Bowenoid cervical CA papulosis and anogenital cancer cytolytic activity of NK cells containing HPV-16 keratinocyte decline may be caused by defects in the identification of disease-specific target cells, keratinocytes did not express MHC Ⅱ antigen (HLA-DR), no such antigen-presenting function can undermine the role of immune surveillance.

    Second, the humoral immune

    Serological testing results show that: (1) anti-late protein antibody generation rate of 25% -65%, compared with anti-early protein high antibody production; (2) detected HPV antibodies may have type-specific, and no cross-reaction; ③ anti-HPV- 16E7 is closely related to the presence of antibodies and cervical cancer; ④ anti-HPV-16E4 the antibody also the occurrence of cervical cancer, signs of recurrence or recent HPV infection; ⑤ adults and children is estimated to produce the same positive rate of IgG antibodies, different type positive rate in 10 % -75% between; ⑥ that HPV-16 or 18-type tumor antibody-positive patients, only 50% -70% of the antibody can be detected.

    Third, genital warts natural healing

    CA spontaneous regression is no systematic assessment, placebo-controlled study found, however, in its spontaneous regression rate of 0%, 17%, 18% and 69%, CA subside or cure, there are still 45% of patients with latent infection 67% of patients with relapsed.