Human papillomavirus infection (viral warts, genital warts, venereal kondilomatoz) - a group of viral infectious disease characterized by the development papillomatoznyh formations on the skin and mucous membranes, chronic relapsing course, widespread, highly contagious. Human papillomavirus (HPV infection, PVI) is one of the most common urogenital viral infections, sexually transmitted diseases, notable for the diversity of its clinical manifestations.
Pathogen - a group of DNA-containing viruses of the family Papavaviridae (Human Papilloma Virus, HPV). Currently identified more than 100 types of HPV are described in detail more than 70 types of HPV, firmly established the fact that certain types of HPV can infect a strictly defined type of epithelium and cause specific changes.
Papillomavirus types 6, 11, 16, 18 and 33 cause genital infections, perianal area, rarely found in the mucous membranes of the mouth of the bladder. Papillomavirus type 6 (a, b, c, d, e) isolated from giant condyloma Buschke-Loewenstein and cervical dysplasia. Papillomavirus types 5a, 5b, 8 cause the development of malignant epidermodysplasia verruciformis. In patients with secondary immunodeficiency in the skin lesions common type 8. In laryngeal papillomas are HPV types 6, 11, 16, 30.
Source papillomavirus infection: a man. HPV transmission: through direct contact of skin or mucous membranes, including sexual contact. In 50-70% of infants born to mothers infected with papilloma virus, is the vertical transmission of the virus. Autoinokulyatsiya papillomavirus possible emergence of new papillomas beyond primary education.
Susceptibility to human papillomavirus high, the disease is widespread. The incubation period of HPV: from 1 to 5 months.
Clinical signs of HPV varies depending on the type of virus and localization of structures. Morphologically education constitute a papilloma with a wide or thin a basis, on the eyelids, neck - in the form of filamentous outgrowths. In normal and plantar warts pronounced thickening and excessive keratinization of the surface layers of cells. Genital warts anomalies of the genital area is usually soft, lobed, heavily vaskulyarizovannye in the leg a lymphocytic infiltration. It is known that in chronic mechanical stimulation (rubbing) warts can reach 3-5 cm in diameter. Papillomavirus GENITAL
Genital HPV infection is currently allocated to a particular group. For many years it was assumed that normal, flat (juvenile) and genital warts are caused by one type of HPV, and the differences in the clinical course due to differences in localization. Views on the pathology of genital kondilomatoza were radically revised after Meisels, Fortin (1976), Purola, Savia (1976) described the genital flat and inverted (endophytic) warts, defining their fundamental difference from warts at other sites, and postulated the cytomorphological features of human papillomavirus infection : koilotsitoz or ballonirovanie cells, characterized by an increase, hyperchromic nuclei, surrounded by a clear zone of light cytoplasm. Koss, Durfee (1956) introduced into clinical practice, the term "koylotsitoticheskaya atypia. The authors first noted the relationship between koylotsitoticheskoy atypia. dysplasia and cervical cancer.
Of all the identified types of HPV 34 are associated with anogenital lesions. Papilloma viruses infect the basal layers of epithelium (the most "sensitive" areas is the transition zone of stratified squamous epithelium in the cylindrical epithelium). Genital warts are often multiple, during pregnancy or in the background inflammatory process tend to have rapid growth and dissemination. Caused by papilloma viruses pathomorphological changes Kurz (1993) and Schiffman (1994) are classified as:
Cell lines derived from tumors, and biopsies of abnormal tissue has long remained the only material for studying the mechanisms of HPV. Failure of reproduction papillomavirus in cell culture, the lack of conclusive serological tests for viral infection, the variety of manifestations of cytopathic effects of virus and the subjectivity of assessment and interpretation of virus-induced cytological and histopathological changes hindered further investigation.
For the first time serious assumptions about the possible role of HPV in cervical cancer development were expressed in the mid 70's. It should be emphasized that the definition of a virus as an etiological factor in tumor development "is based on a combination of the following criteria:
Oncogenic potential of papillomaviruses vary considerably: the ability to initiate dysplastic (precancerous) changes in cancer and papillomaviruses arbitrarily divided into groups of "high" and "low" risk of malignant transformation of infected epithelial cells. Types of HPV 6.11, 42, 43, 44 were classified as low-risk types of cancer, HPV types 16, 18, 48, 56 - high risk. Thus, papillomaviruses types 6 and 11 cause genital warts, often identified with mild dysplasia and moderate severity and rarely associated with tumors of the uterine cervix. HRV type 16 and 18 prevail over other types of papillomaviruses in cervical cancer, papilloma viruses type 16 is detected in 50-70% of cases, 10-20% of detected papillomavirus type 18, other types of high-risk HPV detected much less frequently.
Most frequently identified HPV 16 type, it was revealed in 21% CIN-I, in 57% of CIN-II-III. Since HPV infection types 16 and 18 associated 67-93% of cases of cervical cancer, HPV type 18 is found approximately 2 times less papillomavirus type 16. Papillomavirus type 18 is associated with the development of adenocarcinoma has a higher oncogenic potential, with associated rapid rate of tumor progression, the low level of differentiation of infected epithelial prognosis than other oncogenic HPV types.
Laboratory diagnosis of papillomavirus: the most sensitive method currently recognized by the polymerase chain reaction (PCR) with type-specific and species-specific primers, allowing to detect HPV viral genome, including viral sequences in the genome of tumor cells of the cervix in 95-100% of cases.