Author(s): Georgieva S, Iordanov V, Sergieva S
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Abstract Papillomaviruses are small DNA viruses that infect and multiply in cutaneous or mucosal epithelial tissue. Human papillomavirus (HPV) 16 and 18 cause more than 99\% of cervical carcinomas. Simultaneous presence of HPV is found in cervical intraepithelial neoplasia, vaginal intraepithelial neoplasia, vaginal and anal cancer. Invasive vulvar squamous cell carcinoma in younger women under the age of 50 are also associated with HPV. Most of the penile lesions are subclinical and the high prevalence of high-risk HPV suggests that they constitute a reservoir for high-risk HPV. Bowens disease and Buschke-Lowenstein tumors are associated with particular low- and high-risk HPV types. The potential role of HPV infection in the carcinogenic steps of breast, prostate, colorectal and lung cancers should be further tested. HPV-DNA might be transported from the original site of infection to the breast tissue by the bloodstream, and therefore is possibly involved in the carcinogenesis of breast neoplasia in some patients. HPV-DNA is detected in 40-70\% of head and neck squamous cell carcinomas and in only 1\% in normal epithelial cells. In this paper we propose the hypothesis that many epithelial normal cells are susceptible to HPV infection, which are the most sexually transmitted viruses. Experimental and epidemiological data imply a causative role for HPVs and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage.
This article was published in J BUON
and referenced in Journal of Neurological Disorders