Figure 5. Natural history and pathogenesis of zoster.

The classic mod el of zoster pathogenesis first described by Hope-Simpson²⁰ links viral replication and clinical disease with the levels of cell-mediated immunity (CMI). In primary infection, no immunity to varicella zoster virus (VZV) exists and infection becomes apparent as varicella. CMI then controls replication, and reactivation of the virus remains subclinical and asymptomatic (‘contained reversions’). Exogenous contact with VZV can boost CMI; nevertheless, CMI levels decrease over time and when they fall below a critical level, zoster can develop. Adapted with permission from REF 20, The Royal Society of Medicine.