aricella-zoster virus (VZV) is a ubiquitous human alpha- herpesvirus, which causes varicella (chicken pox) and herpes zoster (shingles). Varicella results from primary VZV infec- tion; it is a common childhood illness associated with fever and a generalized pruritic vesicular rash. As is characteristic of the alphaherpesviruses, VZV establishes latency in cells of the dorsal root ganglia after primary infection. Herpes zoster is a localized, painful, vesicular rash involving one or adjacent der- matomes and caused by VZV reactivation. The incidence of herpes zoster increases with age or immunosuppression.
Historically, the relationship between the etiologies of vari- cella and herpes zoster was first suggested by von Bo ́kay in 1892, from the observation that young children often devel- oped varicella after exposure to an adult with herpes zoster (249). Transmissibility of the agent was demonstrated by inoc- ulating children who had no history of varicella with fluid recovered from herpes zoster lesions; these children developed varicella, and secondary
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Goodpasture and Anderson detected multinucleated giant cells in a human skin/ chorioallantoic membrane culture system infected with herpes zoster lesion fluid in 1944 (107), and infectious VZV was isolated in tissue culture by Weller and Stoddard in 1953 (258). Knowledge about the molecular virology of VZV and mecha- nisms of pathogenicity has grown during the past two decades. The complete VZV genome has been sequenced, the infectiv- ity of intact VZV DNA has been demonstrated (39, 53), and, most recently, infectious virus has been produced from cos- mids spanning the genome (39). Antiviral agents that modify the severity of varicella and herpes zoster have been devel- oped, and a live attenuated varicella vaccine that protects against primary VZV infection is now licensed for clinical use (3, 245, 260,