Simian varicella virus pathogenesis

Abstract

Because varicella zoster virus (VZV) is an exclusively human pathogen, the development of an animal model is necessary to study pathogenesis, latency, and reactivation. The pathological, virological, and immunological features of simian varicella virus (SVV) infection in nonhuman primates are similar to those of VZV infection in humans. Both natural infection of cynomolgus and African green monkeys as well as intrabronchial inoculation of rhesus macaques with SVV provide the most useful models to study viral and immunological aspects of latency and the host immune response. Experimental immunosuppression of monkeys latently infected with SVV results in zoster, thus providing a new model system to study how the loss of adaptive immunity modulates virus reactivation.

Fig. 1

Detection of VZV and SVV ORF 63 proteins in the cytoplasm of neurons in ganglia of a human latently infected with VZV and a rhesus macaque latently infected with SVV. Paraformal-dehyde-fixed, paraffin-embedded sections of thoracic ganglia from a VZV seropositive 46-year-old man (a) (Mahalingam et al. 1996) and from a rhesus macaque latently infected with SVV (b) (Messaoudi et al. 2009) were analyzed by immunohistochemistry using rabbit anti-VZV ORF 63. Both VZV and SVV ORF 63 proteins are located exclusively in the cytoplasm of neurons in the respective ganglia. The arrows indicate the location of ORF 63 protein in the neuronal cytoplasm. Figure 1a reprinted with permission of National Academy of Sciences, USA (Mahalingam et al. (1996); Copyright 1996 National Academy of Sciences. USA); and Fig. 2b PLoS pathogens (Messaoudi et al. 2009)