Mucosal human papillomavirus (HPV) infections are the most common sexually transmitted disease (STD). When clinically symptomatic, lesions are barely visible papules to nodules to confluent masses occurring on anogenital or oral mucosa or skin, caused by infection with a mucosal type of HPV. Only 1 to 2% of HPV-infected individuals have any visibly detectable clinical lesion. HPV present in the birth canal can be transmitted to a newborn during vaginal delivery and can cause external genital warts (EGW) and respiratory papillomatosis. HPV dysplasia of the anogenital skin and mucosa ranging from mild to severe to squamous cell carcinoma (SCC) in situ (SCCIS); invasive SCC can arise within SCCIS, most commonly in the cervix and anal canal.
"Low-risk" and "high-risk" HPV types both cause EGW. HPV infection probably persists throughout a patient's lifetime in a dormant state and becomes infectious intermittently. Exophytic warts are probably more infectious than subclinical infection.
Immunosuppression results in new expression of HPV lesions, progression of HPV lesions, no increased rate of HPV infection but an increased risk of transmission, increased multifocal intraepithelial neoplasia. Immunosuppressed renal transplant recipients have a 17-fold greater incidence of genital HPV infection.
All HPV types replicate exclusively in host's cell nucleus. In benign HPV-associated lesions, HPV exists as a plasmid in cell's cytoplasm, replicating extrachromosomally. In malignant HPV-associated lesions, HPV integrates into host's chromosome, following a break in the viral genome (around E1/E2 region). E1 and E2 function is deregulated, resulting in cellular transformation.
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