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Both viruses cause varicella as a primary infection, establish latency in ganglionic neurons and reactivate later in life to cause herpes zoster in their respective hosts. <jats:styled-content style=\"fixed-case\">VZV<\/jats:styled-content> is endemic worldwide and, although varicella is usually a benign disease in childhood, <jats:styled-content style=\"fixed-case\">VZV<\/jats:styled-content> reactivation is a significant cause of neurological disease in the elderly and in immunocompromised individuals. The pathogenesis of <jats:styled-content style=\"fixed-case\">VZV<\/jats:styled-content> infection remains ill\u2010defined, mostly due to the species restriction of <jats:styled-content style=\"fixed-case\">VZV<\/jats:styled-content> that impedes studies in experimental animal models. <jats:styled-content style=\"fixed-case\">SVV<\/jats:styled-content> infection of non\u2010human primates parallels virological, clinical, pathological and immunological features of human <jats:styled-content style=\"fixed-case\">VZV<\/jats:styled-content> infection, thereby providing an excellent model to study the pathogenesis of varicella and herpes zoster in its natural host. In this review, we discuss recent studies that provided novel insight in both the virus and host factors involved in the three elementary stages of <jats:italic>Varicellovirus<\/jats:italic> infection in primates: primary infection, latency and reactivation. Copyright \u00a9 2014 Pathological Society of Great Britain and Ireland. 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