An Animal Model of Varicella Virus Infection

@article{White2001AnAM,
  title={An Animal Model of Varicella Virus Infection},
  author={Tiffany M. White and Donald H. Gilden and Ravi Mahalingam},
  journal={Brain Pathology},
  year={2001},
  volume={11}
}
Varicella‐zoster virus (VZV) causes chickenpox in children; establishes latency in cranial nerve, dorsal root, and autonomic ganglia; and reactivates decades later to produce zoster. VZV produces disease only in humans. Although attempts to produce disease and study VZV latency in experimentally infected animals have resulted in virus in trigeminal or dorsal root ganglia, no clinical signs of infection or reactivation developed. In contrast, simian varicella virus (SVV) produces a naturally… Expand
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Simian varicella: a model for human varicella‐zoster virus infections
  • W. Gray
  • Biology, Medicine
  • Reviews in medical virology
  • 2004
TLDR
The relatedness of VZV and SVV and the similarities in the clinical symptoms and pathogenesis of human and simian varicella make SVV infection of nonhuman primates an excellent animal model to investigate V zoster pathogenesis and latency, and to evaluate potential antiviral strategies. Expand
Insights into the Pathogenesis of Varicella Viruses
TLDR
The immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster are examined. Expand
Clinical and molecular pathogenesis of varicella virus infection.
TLDR
A current summary ofvaricella latency and pathogenesis produced by simian varicella virus (SVV), the counterpart of human VZV, points to the usefulness of a primate model of natural infection to study variceLLA latency, as well as the experimental model of intratracheal inoculation to study the effectiveness of antiviral agents in driving persistent variceella virus into a latent state. Expand
Simian Varicella Virus Infection of Rhesus Macaques Recapitulates Essential Features of Varicella Zoster Virus Infection in Humans
TLDR
Intrabronchial inoculation of rhesus macaques with SVV provides a novel model to analyze viral and immunological mechanisms of VZV latency and reactivation and presents the first in depth analysis of the immune response to SVV. Expand
Varicella zoster virus latency, neurological disease and experimental models: an update.
TLDR
Since neurological disease produced by VZV is due to reactivation from ganglia, the physical state of viral nucleic acid and expression during latency as well as the possible mechanisms by which VZv latency is maintained and reactivates are discussed. Expand
Viral gene expression during acute simian varicella virus infection.
TLDR
This study demonstrates expression of specific SVV immediate early, early and late genes in the skin, lung, liver and ganglia tissues of acutely infected monkeys and provides a foundation for further investigation on the role of viral genes in varicella pathogenesis and latency. Expand
Simian varicella virus: molecular virology.
  • W. Gray
  • Biology, Medicine
  • Current topics in microbiology and immunology
  • 2010
TLDR
Genetic approaches have been developed to create SVV mutants, which will be used to study the role of SVV genes in viral pathogenesis, latency, and reactivation, and foreign genes are being investigated as potential recombinant varicella vaccines. Expand
A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.
TLDR
There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated, and in vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms hold much promise for the future understanding in this complex area. Expand
Human trigeminal ganglionic explants as a model to study alphaherpesvirus reactivation
Varicella zoster virus (VZV) latency is characterized by limited virus gene expression and the absence of virus DNA replication. Investigations of VZV latency and reactivation have been hindered by… Expand
Varicella-Zoster Virus Gene 66 Transcription and Translation in Latently Infected Human Ganglia
TLDR
Analysis of latently infected human trigeminal ganglia for 66-pk expression by reverse transcriptase-dependent nested PCR revealed VZV open reading frame 66 to be a previously unrecognized latently expressed virus gene and suggests that prevention of IE62 import to the nucleus by VZ V 66- pk phosphorylation is one possible mechanism by which VZv latency is maintained. Expand
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