Abstract
Simian varicella virus (SVV) causes a natural varicellaβlike disease in nonhuman primates. Epizootics of simian varicella occur sporadically in facilities housing Old World monkeys. SVV is antigenically and genetically related to varicellaβzoster 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%β75% DNA homology and are coβlinear 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 lifeβlong 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. Copyright Β© 2004 John Wiley & Sons, Ltd.