Pathogenesis

The transmission of herpes simplex virus (HSV) infection is dependent upon intimate, personal contact of a susceptible seronegative individual with someone excreting HSV. Virus must come in contact with mucosal surfaces or abraded skin for infection to be initiated. With viral replication at the site of primary infection, either an intact virion or, more simply, the capsid is transported retrograde by neurons to the dorsal root ganglia where, after another round of viral replication, latency is established (Fig. 32.1(a), left panel). The more severe the primary infection, as reflected by the size, number, and extent of lesions, the more likely it is that recurrences will ensue. Although replication sometimes leads to disease and, infrequently, results in life-threatening infection (e.g., encephalitis), the host-virus interaction leading to latency predominates. After latency is established, a proper stimulus causes reactivation; virus becomes evident at mucocutaneous sites, appearing as skin vesicles or mucosal ulcers (Fig. 32.1(b), right panel).

Infection with HSV-1 generally occurs in the oropharyngeal mucosa. The trigeminal ganglion becomes colonized and harbors latent virus. However, it has been increasingly common to detect evidence of HSV-1 in the genital tract, usually the consequence of oral-genital sex. When such occurs, recurrences of HSV-1 in the genital tract are uncommon. Acquisition of HSV-2 infection is usually the consequence of transmission by genital contact. Virus replicates in the genital, perigenital or anal skin sites with seeding of the sacral ganglia (Fig. 32.2).