Varicella-zoster Virus

Volume 342 of the series Current Topics in Microbiology and Immunology pp 211-228


Experimental Models to Study Varicella-Zoster Virus Infection of Neurons

  • Megan SteainAffiliated withDepartment of Infectious Diseases and Immunology, University of Sydney
  • , Barry SlobedmanAffiliated withCentre for Virus Research, Westmead Millennium Institute
  • , Allison AbendrothAffiliated withDepartment of Infectious Diseases and Immunology, University of Sydney Email author 

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Varicella zoster virus (VZV) infection results in the establishment of latency in human sensory neurons. Reactivation of VZV leads to herpes zoster which can be followed by persistent neuropathic pain, termed post-herpetic neuralgia (PHN). Humans are the only natural host for VZV, and the strict species specificity of the virus has restricted the development of an animal model of infection which mimics all phases of disease. In order to elucidate the mechanisms which control the establishment of latency and reactivation as well as the effect of VZV replication on neuronal function, in vitro models of neuronal infection have been developed. Currently these models involve culturing and infecting dissociated human fetal neurons, with or without their supporting cells, an intact explant fetal dorsal root ganglia (DRG) model, neuroblastoma cell lines and rodent neuronal cell models. Each of these models has distinct advantages as well as disadvantages, and all have contributed towards our understanding of VZV neuronal infection. However, as yet none have been able to recapitulate the full virus lifecycle from primary infection to latency through to reactivation. The development of such a model will be a crucial step towards advancing our understanding of the mechanisms involved in VZV replication in neuronal cells, and the design of new therapies to combat VZV-related disease.