Clinical Infectious Disease

The virus

Herpesviruses are generally defined as large enveloped virions with an icosapentahedral nucleocapsid consisting of 162 capsomeres arranged around a double-stranded DNA core. The two antigenically distinct types of herpes simplex virus (HSV) are HSV-1 and HSV-2. Considerable homology exists between the HSV-1 and HSV-2 genomes, with most of the polypeptides specified by one viral type being antigenically related to polypeptides of the other viral type. Although this results in considerable cross-reactivity between the HSV-1 and HSV-2, glycoproteins G (gG) are unique antigenic determinants that allow for differentiation between these two viruses (e.g., gG-1 and gG-2). Surrounding the viral genome and nucleocapsid is a tightly adherent membrane known as the tegument. A lipid envelope containing the viral glycoproteins loosely surrounds the tegument.

Pathology and pathogenesis

Cutaneous HSV infection causes ballooning of infected epithelial cells, with nuclear degeneration, loss of intact cellular membranes, and the formation of multinucleated giant cells. Ultimately, cells lyse and release clear fluid containing large quantities of virus, with subsequent accumulation of cellular debris and inflammatory cells between the epidermal and dermal layers. Multinucleated giant cells are usually present at the base of the vesicle. An intense inflammatory response extends from the base of the vesicle into the dermis, producing the erythema that classically surrounds a cluster of HSV vesicles. As the lesions heal, vesicular fluid becomes purulent as more inflammatory cells are recruited to the site of infection. Scab formation then follows. Scarring is uncommon.