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INTRODUCTION

Herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) are 2 of the 8 members of the human herpesvirus family. Along with varicella-zoster virus (VZV), HSV-1 and HSV-2 belong to the alpha-herpesvirus subfamily and share the characteristic neurotropism and establishment of latency in sensory ganglia, with lifelong infection, periodic reactivation, and reappearance of infectious virus at mucocutaneous sites. Clinical manifestations when present can range from minor mucocutaneous vesicles to hemorrhagic encephalitis or disseminated disease, but most persons infected with either HSV-1 or HSV-2 are asymptomatic (Table 304-1).

TABLE 304-1INFECTIONS CAUSED BY HUMAN HERPESVIRUSES

PATHOGENESIS AND EPIDEMIOLOGY

Herpes simplex viruses are 150 to 200 nm in diameter and consist of a core of linear double-stranded DNA surrounded by an icosahedral capsid, a fibrillous tegument, and a lipid envelope containing viral glycoprotein spikes that mediate attachment and entry into host cells and are responsible for evoking the host response.

There is extensive homology between HSV-1 and HSV-2, rendering serologic distinction difficult. There are at least 60 proteins specified by the virus. Mucocutaneous epithelial cells provide the presumed initial target for viral infection, whereas neural cells in trigeminal and sacral root ganglia constitute the site of latent infection.

Infection of the susceptible host results when herpes simplex virus penetrates through abraded skin or mucosal surfaces. After minimal local replication at the site of inoculation, virus migrates along innervating axons to the sensory ganglia where infectious virus is synthesized. Visible lesions result after the virus returns to the inoculation site via peripheral sensory nerves. Vesicular lesions appear between epidermal and dermal layers and contain large amounts of virus, cell debris, and inflammatory cells. When the host is unable to limit viral replication, such as in newborns and the immunocompromised, viremia may result in multiorgan ...

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