Herpes zoster (HZ, shingles) is caused by the reactivation of latent varicella zoster virus (VZV) and causes significant morbidity and sometimes mortality in the elderly. Several clinical studies suggest that the waning of T cell immunity with age is the underlying cause of VZV reactivation. However, the exact defects in T cell immunity remain poorly understood due to the fact that VZV infection of laboratory animals, including nonhuman primates, does not result in disease. We have developed a novel animal model wherein rhesus macaques are inoculated with the closely related simian varicella virus (SVV). SVV infection of rhesus macaques reproduces hallmarks of VZV infection in humans: 1) generalized varicella; 2) the development of cellular and humoral immunity; and 3) the establishment of latency with limited transcriptional activity in sensory ganglia. This is the only model where acute infection and latency can be studied in the same animal. Furthermore, whereas adult rhesus macaques can resolve acute SVV infection, aged animals remain persistently viremic. The SVV-specific antibody response generated by elderly animals was comparable to that of adult animals. On the other hand, the SVV-specific T cell response in aged animals was delayed and reduced in magnitude. These data suggest that, similar to clinical observations about VZV, the inability of aged animals to control SVV viremia is due to a reduced T cell response.