• Wayne L Gray.
• Department of Microbiology and Immunology, 4301 West Markham Street, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA. graywayne1@uams.edu
• Rev. Med. Virol. 2004 Nov 1; 14 (6): 363-81.

AbstractSimian varicella virus (SVV) causes a natural varicella-like disease in nonhuman primates. Epizootics of simian varicella occur sporadically in facilities housing Old World monkeys. SVV is antigenically and genetically related to varicella-zoster virus (VZV), the etiologic agent of varicella (chickenpox) and herpes zoster (shingles) in humans. The SVV and VZV genomes are similar in size and structure, share 70%-75% DNA homology and are co-linear with respect to gene organisation. Simian varicella is a highly contagious disease characterised by fever and vesicular skin rash and may progress to pneumonia and hepatitis. Infected monkeys may resolve the disease within 2 weeks although epizootics are sometimes associated with high morbidity and mortality. SVV, like VZV, establishes life-long latent infection, as indicated by detection of viral DNA within neural ganglia. Subsequently, SVV may reactivate to cause secondary disease and spread of the virus to susceptible monkeys. 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 VZV pathogenesis and latency, and to evaluate potential antiviral strategies.2004 John Wiley & Sons, Ltd.

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