Varicella Zoster Virus Neuropathogenesis and Latency
Donald H. Gilden, Ravi Mahalingam, Steven Deitch, and Randall J. Cohrs
from: Alpha Herpesviruses: Molecular and Cellular Biology (Edited by: R. M. Sandri-Goldin). Caister Academic Press, U.K. (2006)
Varicella zoster virus (VZV) is a highly neurotropic alphaherpesvirus. VZV causes chickenpox in 4 million children in the United States annually, after which virus becomes latent in cranial nerve, dorsal root and autonomic nervous system ganglia along the entire neuraxis. Decades later, a declining VZV host immunity allows virus to reactivate spontaneously, resulting in zoster, the primary neurologic complication of VZV reactivation, characterized by pain and rash restricted to 1-3 dermatomes. This chapter reviews the clinical features of zoster, including the two most serious neurologic complications: postherpetic neuralgia (PHN) and VZV vasculopathy. Evidence is presented to support the notion that VZV vasculopathy and PHN as well, may be caused by persistent virus infection. The chapter also provides an update on the physical state of VZV during latency in human ganglia, including the distribution and prevalence of virus in ganglia, virus abundance and configuration, cell type infected, and extent of virus transcription and translation. Finally, because VZV is an exclusively human virus, no animal model of latency and reactivation has been achieved. However, simian varicella virus (SVV), the primate counterpart of human VZV, does produce chickenpox and reactivate in monkeys. The chapter provides an update of studies, which have used SVV in primates as a model to study varicella latency and persistence read more ...