Varicella Zoster Virus in the Nervous System

Abstract

Varicella zoster virus (VZV) is a ubiquitous, exclusively human alphaherpesvirus. Primary infection usually results in varicella (chickenpox), after which VZV becomes latent in ganglionic neurons along the entire neuraxis. As VZV-specific cell-mediated immunity declines in elderly and immunocompromised individuals, VZV reactivates and causes herpes zoster (shingles), frequently complicated by postherpetic neuralgia. VZV reactivation also produces multiple serious neurological and ocular diseases, such as cranial nerve palsies, meningoencephalitis, myelopathy, and VZV vasculopathy, including giant cell arteritis, with or without associated rash. Herein, we review the clinical, laboratory, imaging, and pathological features of neurological complications of VZV reactivation as well as diagnostic tests to verify VZV infection of the nervous system. Updates on the physical state of VZV DNA and viral gene expression in latently infected ganglia, neuronal, and primate models to study varicella pathogenesis and immunity are presented along with innovations in the immunization of elderly individuals to prevent VZV reactivation.

Keywords: Giant Cell Arteritis; Immunization; Latency; VZV; Varicella zoster virus; Vasculopathy.

Figure 1.. Detection of varicella zoster virus (VZV) antigen in the temporal artery of a patient with giant cell arteritis.

Hematoxylin-and-eosin staining of the temporal artery from a 90-year-old man with classic giant cell arteritis ( A). Note extensive inflammation in the adventitia, media and intima, disruption of the media, a thickened intima, and nearly occluded arterial lumen; inset denotes a giant cell. Immunohistochemical staining with mouse anti-VZV gE antibody revealed VZV antigen (red) in the adventitia and media of the temporal artery ( B) that was not seen when mouse isotype IgG1 antibody was substituted for mouse anti-VZV gE antibody ( C).