Introduction

All herpes viruses can establish a persistent state after primary infection.

Persons who become infected with a herpesvirus are susceptible to periodic viral reactivation releasing transmissible virus. The latent sites determine clinical manifestations and are variable. HSV-1, HSV-2, and VZV have structure and propensity similar to all members of the herpesvirus family. The double-stranded DNA genome is surrounded by a nucleocapsid and becomes dormant and persistent in the nucleus of sensory cells. Although circulating antibodies are present in both diseases, HSV antibodies are not protective: Reactivation is common, and recurrence is not accompanied by increase in the quantity of circulating antibodies. HSV reactivation with replication produces secondary neurocuta-neous disease or may manifest as asymptomatic viral shedding (5,6).

In VZV infection, the antibodies remain protective until later in life, when antibody protection is lost and recurrence manifests as segmental neurocutaneous disease ("shingles") with a concomitant rise in antibodies. VZV rarely recurs a second time. Another factor common to HSV and VZV is that both viruses are responsible for syndromes affecting multiple nerves and dermatomes.

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