Primary infection with varicella zoster virus (VZV) causes chickenpox (varicella) after which virus becomes latent in cranial nerve, dorsal root and autonomic ganglia along the entire neuraxis. Virus may later reactivate, causing shingles (zoster), characterized by pain and rash restricted to 1–3 dermatomes. More than 40% of zoster patients over age 60 develop postherpetic neuralgia (PHN), pain that persists for months to years. The socioeconomic impact of primary varicella infection has been lessened by introduction of VZV vaccine for children. However, the effect of childhood vaccination on the incidence of zoster is unknown. Virus reactivation correlates with waning cell-mediated immunity (CMI) to VZV with normal aging. Adults exposed to children with varicella may have a boost in CMI to VZV. For at least several more decades, the incidence of zoster may increase as the elderly population grows. The anticipated increase in zoster burden of illness in future decades was a major impetus for the Shingles Prevention Study, a prospective, double-blind, placebo-controlled trial of attenuated VZV vaccine to prevent zoster in older adults. This review discusses clinical and virological aspects of zoster and its complications, current treatment options, and VZV vaccine development along with its future role in disease prevention.