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Current In Vitro Models to Study Varicella Zoster Virus Latency and Reactivation
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Current In Vivo Models of Varicella-Zoster Virus Neurotropism

Department of Neurology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA
Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Pediatric Infectious Disease, Stanford University, Stanford, CA 94305, USA
Department of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers University, Newark, NJ 07102, USA
Biology Department, University of Mississippi, Oxford, MS 38677, USA
Departments of Molecular Biology and Biochemistry, School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USA
Division of Microbiology, Tulane University, Tulane National Primate Research Center, Covington, LA 70433, USA
Author to whom correspondence should be addressed.
Viruses 2019, 11(6), 502;
Received: 1 February 2019 / Revised: 24 April 2019 / Accepted: 28 May 2019 / Published: 31 May 2019
(This article belongs to the Special Issue Varicella Zoster Virus)
Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce zoster and associated neurological complications. An understanding of VZV neurotropism in humans has long been hampered by the lack of an adequate animal model. For example, experimental inoculation of VZV in small animals including guinea pigs and cotton rats results in the infection of ganglia but not a rash. The severe combined immune deficient human (SCID-hu) model allows the study of VZV neurotropism for human neural sub-populations. Simian varicella virus (SVV) infection of rhesus macaques (RM) closely resembles both human primary VZV infection and reactivation, with analyses at early times after infection providing valuable information about the extent of viral replication and the host immune responses. Indeed, a critical role for CD4 T-cell immunity during acute SVV infection as well as reactivation has emerged based on studies using RM. Herein we discuss the results of efforts from different groups to establish an animal model of VZV neurotropism. View Full-Text
Keywords: varicella zoster virus; animal models; simian varicella virus varicella zoster virus; animal models; simian varicella virus
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Mahalingam, R.; Gershon, A.; Gershon, M.; Cohen, J.I.; Arvin, A.; Zerboni, L.; Zhu, H.; Gray, W.; Messaoudi, I.; Traina-Dorge, V. Current In Vivo Models of Varicella-Zoster Virus Neurotropism. Viruses 2019, 11, 502.

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