Abstract
Primary infection with varicella zoster virus (VZV) results in varicella (chickenpox) followed by the establishment of latency in sensory ganglia. Declining T cell immunity due to aging or immune suppressive treatments can lead to VZV reactivation and the development of herpes zoster (HZ, shingles). HZ is often associated with significant morbidity and occasionally mortality in elderly and immune compromised patients. There are currently two FDA-approved vaccines for the prevention of VZV: Varivax® (for varicella) and Zostavax® (for HZ). Both vaccines contain the live-attenuated Oka strain of VZV. Although highly immunogenic, a two-dose regimen is required to achieve a 99% seroconversion rate. Zostavax vaccination reduces the incidence of HZ by 51% within a 3-year period, but a significant reduction in vaccine-induced immunity is observed within the first year after vaccination. Developing more efficacious vaccines and therapeutics requires a better understanding of the host response to VZV. These studies have been hampered by the scarcity of animal models that recapitulate all aspects of VZV infections in humans. In this review, we describe different animal models of VZV infection as well as an alternative animal model that leverages the infection of Old World macaques with the highly related simian varicella virus (SVV) and discuss their contributions to our understanding of pathogenesis and immunity during VZV infection.
Highlights
Successful infection of guinea pigs with varicella zoster virus (VZV) only occurs with the use of a guinea pig-adapted strain [45], which is prepared by passaging the virus 10–30 times in fetal guinea pig cells [46,47,48,49] and in some cases is further propagated in human diploid cells [50]
Our understanding of VZV biology has increased substantially since it was first discovered over a century ago
The ability of VZV to establish latency in sensory ganglia of these animals offers an opportunity to identify viral genes that are critical to the establishment and/or maintenance of viral latency
Summary
Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus of the Varicellovirus genus, and the causative agent of varicella (chickenpox) and herpes zoster (HZ, shingles). Like other members of the alphaherpesvirus subfamily, VZV establishes a latent infection in sensory ganglia [1]. The structure of VZV is indistinguishable from other herpesviruses and is comprised of four main elements: the core, the nucleocapsid, the tegument, and the envelope [1]. The unstructured proteinaceous layer between the nucleocapsid and envelope is called the tegument and contains an assortment of viral proteins believed to modulate the host environment to meet the needs of the virus [3]. VZV encodes 70 unique open reading frames (ORFs) [6] and viral gene transcription during lytic infection appears to be coordinated and follows a temporal program with immediate-early, early, and late genes [7]
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