Varicella-Zoster Virus: One Pathogen With Multifaceted Imaging and Clinical Manifestations Influenced by Varied Pathophysiologic Mechanisms of Dissemination

Varicella-zoster virus is a ubiquitous, exclusively human, neurotropic virus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Varicella-zoster virus reactivation, primarily in elderly individuals and individuals who are immunocompromised, produces herpes zoster. During their lifetime, up to one-third of people will develop zoster, often complicated by diverse neurologic and ocular disorders. Imaging is helpful, particularly because these manifestations can occur without a rash. Live attenuated varicella-zoster virus vaccine prevents varicella, although the vaccine virus becomes latent and reactivates to cause zoster just as wild-type varicella-zoster virus does. To prevent zoster, a more potent preparation of live attenuated virus was created, which boosts cell-mediated immunity to varicella-zoster virus and reduces the incidence of zoster and postherpetic neuralgia for years after immunization. But the long-term effectiveness of immunization after age 60 years is unknown. This review discusses varicella-zoster virus epidemiology and pathophysiology, and vaccines to prevent varicella and zoster, and provides a foundation for understanding when the disease is likely to occur and what imaging features predominate. An organizational chart is presented with selected illustrative imaging cases that demonstrate the protean neurologic manifestations of varicella-zoster virus infection of the nervous system.

Learning Objective: Describe the epidemiology and pathologic processes responsible for the multifaceted imaging findings and affected clinical populations associated with VZV reactivation.