Etiology and Epidemiology
ETIOLOGY HPV is a DNA papovavirus that multiplies in the nuclei of infected epithelial cells (see Section 27). More than 20 types of HPV can infect the genital tract: types 6, 11 most commonly. Types 16, 18, 31, 33, and 35 are strongly associated with anogenital dysplasia and carcinoma. In persons with multiple sexual partners, subclinical infection with multiple HPV types is common.
RISK FACTORS FOR ACQUIRING HPV INFECTION Number of sexual partners/frequency of sexual intercourse. Sexual partner with HPV anogenital infection. Infection with other STIs.
TRANSMISSION Through sexual contact: genital-genital, oral-genital, and genital-anal. Microabrasions occur on the epithelial surface allowing virions from the infected partner to gain access to the basal cell layer of the noninfected partner.
INCIDENCE Most sexually active individuals are subclinically infected with HPV; most HPV infections are asymptomatic, subclinical, or unrecognized. One percent of sexually active adults (15 to 19 years of age) develop clinical lesions.
PATHOGENESIS "Low-risk" and "high-risk" HPV types both cause anogenital infections. HPV infection may persist for years in a dormant state and becomes infectious intermittently. Exophytic warts are probably more infectious than subclinical infection. Immunosuppression may result in new extensive HPV lesions, poor response to treatment, increased multifocal intraepithelial neoplasia. All HPV types replicate exclusively in the host's cell nucleus. In benign HPV-associated lesions, HPV exists as a plasmid in cellular cytoplasm, replicating extrachromosomally. In malignant HPV-associated lesions, HPV integrates into the host's chromosome, following a break in the viral genome (around E1/E2 region). E1 and E2 function is deregulated, resulting in cellular transformation.