Introduction

Varicella-zoster virus (VZV) is a neurotropic human herpesvirus that causes varicella, which is commonly known as chicken pox, as the primary infection in susceptible individuals. In the healthy host, varicella is usually a mild, self-limiting febrile illness characterized by a generalized, pruritic vesicular rash (Figure 12.1A). Like other alphaherpesviruses, VZV gains access to sensory ganglia of the peripheral nervous system during primary infection and establishes lifelong persistence at these sites. VZV reactivation from latency causes herpes zoster, called “shingles,” and is associated with a vesicular rash localized to one of the cutaneous dermatomes of the face, trunk, or extremities (Figure 12.1B). The dermatomal rash reflects the region of skin innervated by the cranial nerve or dorsal root ganglion where reactivation is occurring. VZV is highly contagious and is maintained in the human population by close contact with individuals who have varicella or herpes zoster. Both primary and recurrent VZV infections are more severe in immunocompromised patients because resolution requires an effective cell-mediated immune response. Antiviral drugs that inhibit VZV replication are effective in most high-risk patients with varicella or herpes zoster. VZV is the only human herpesvirus for which vaccines that prevent or modify the severity of primary and recurrent infections have been developed. These vaccines are made from the VZV/Oka strain, attenuated by passage in vitro.

While the clinical manifestations of varicella and herpes zoster are well-documented, knowledge about the mechanisms of VZV pathogenesis in the human host is limited because primary and recurrent infections are rarely fatal and VZV infection is highly species-specific for the human host.