Viral Infections

Introduction
Herpes simplex virus (HSV) is discussed in detail in this articles -Herpes genital (genital Herpes simplex), Herpes Genitalis and Herpes simplex with a brief clinical description outlined in Table 3-16.

Human Papillomavirus

Human papillomavirus (HPV) is a member of the Papovavirus family and is a closed, circular, double-stranded DNA virus. The viral genome is enclosed in an icosahedral capsule composed of several protein capsomeres and lacks the lipid-containing envelope common to many other viruses such as herpes simplex. Unlike other human STD virus infections such as herpes simplex, however, HPV growth in cell culture has been difficult because its replication is dependent on epithelial cell differentiation and maturation.

The common clinical presentation of HPV is the genital wart or external condyloma acuminatum. However, with the advent of DNA amplification techniques, it has become clear that HPV has extensive clinical expression ranging from latency to condyloma to invasive cancers, particularly of the anogenital tract. Subclassification of HPV into over 100 types has been based on differences in degree of DNA homology. Common skin warts are associated with types 2 and 4, whereas benign genital condyloma is usually associated with HPV type 6 or 11. In contrast, anogenital neoplasias are commonly associated with types 16, 18, 31, 33 or 35, 45, and 56.

Pathogenesis
The definitive mechanisms of HPV infection are unclear. The HPV appears to require direct access to basal epithelial cells to establish infection, and active cell division and differentiation are required for HPV replication. Vulnerable human sites where basal cells not only are physically accessible to viral inoculation but also are actively dividing include the active squamous metaplasia of the transformation zone of the female cervix and areas of wound healing in the genital area. In adolescents and young women, 70 to 90% of HPV infections are transient. On the other hand, persistent infection has been closely linked to the development of anogenital cancers. Recent information has linked several viral-host protein interactions with the loss of cell cycle control, a likely step in the development of these cancers. The natural progression from infection to cancer is not well understood. However, cofactors thought to play important roles include HSV, hormonal influences, cigarette smoking, and altered immunologic responses to infection or injury.

Clinical Syndromes
The HPV can cause multicentric disease including much of the anogenital area: the vaginal introitus, vulvar labia minora and majora, clitoris, perineum, anus, and cervix in women; and the penis, including the prepuce, frenulum, corona, glans, and shaft, with the anus and scrotum in men. The common genital warts, condyloma acuminatum, which are seen on the skin surfaces, present as polypoid masses with fissured and irregular surfaces. They are often multiple and polymorphic and commonly coalesce into large masses. When on mucosal surfaces, condyloma acuminatum appears as finger-like projections with central dilated capillary loops.