Introduction

After primary infection (chickenpox) in children, varicella zoster virus (VZV) becomes latent in cranial, dorsal root and autonomic ganglia along the entire neuraxis and may reactivate decades later to produce zoster. The incidence of zoster and its attendant neurological complications is related to a natural decline in cell-mediated immunity (CMI) to VZV that occurs with aging, and which also develops in immunocompromised organ transplant recipients, and patients with cancer or AIDS. Yet the mechanism of reactivation and the cascade of events that are precipitated by impaired CMI to VZV are still unknown. To study such events require an animal model of varicella. While experimental animal models of latency and pathogenesis exist for closely related viruses such as herpes simplex types 1 and 2, VZV causes disease exclusively in humans. Thus, lack of a good animal model has hampered the studies of varicella latency and pathogenesis. Several attempts to produce disease by experimental inoculation of animals have led to seroconversion without clinical symptoms (Takahashi et al., 1975; Myers et al., 1980, 1985; Matsunaga et al., 1982; Wroblewska et al., 1982; Walz-Cicconi et al., 1986). Subcutaneous inoculation of the Oka VZV (vaccine strain) into the breast of a chimpanzee has been shown to produce viremia and mild rash restricted to the site of inoculation (Cohen et al., 1996). VZV DNA was detected in blood mononuclear cells (MNCs) of the chimpanzee during the 10-day incubation period.