Pathogenesis of varicelloviruses in primates

WJD Ouwendijk, GMGM Verjans - The Journal of pathology, 2015 - Wiley Online Library
WJD Ouwendijk, GMGM Verjans
The Journal of pathology, 2015Wiley Online Library
Varicelloviruses in primates comprise the prototypic human varicella‐zoster virus (VZV) and
its non‐human primate homologue, simian varicella virus (SVV). Both viruses cause
varicella as a primary infection, establish latency in ganglionic neurons and reactivate later
in life to cause herpes zoster in their respective hosts. VZV is endemic worldwide and,
although varicella is usually a benign disease in childhood, VZV reactivation is a significant
cause of neurological disease in the elderly and in immunocompromised individuals. The …
Abstract
Varicelloviruses in primates comprise the prototypic human varicella‐zoster virus (VZV) and its non‐human primate homologue, simian varicella virus (SVV). Both viruses cause varicella as a primary infection, establish latency in ganglionic neurons and reactivate later in life to cause herpes zoster in their respective hosts. VZV is endemic worldwide and, although varicella is usually a benign disease in childhood, VZV reactivation is a significant cause of neurological disease in the elderly and in immunocompromised individuals. The pathogenesis of VZV infection remains ill‐defined, mostly due to the species restriction of VZV that impedes studies in experimental animal models. SVV infection of non‐human primates parallels virological, clinical, pathological and immunological features of human VZV infection, thereby providing an excellent model to study the pathogenesis of varicella and herpes zoster in its natural host. In this review, we discuss recent studies that provided novel insight in both the virus and host factors involved in the three elementary stages of Varicellovirus infection in primates: primary infection, latency and reactivation. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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