猴痘病毒发病机制。
Simian varicella virus pathogenesis.
机构信息
Departments of Neurology, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA.
出版信息
Curr Top Microbiol Immunol. 2010;342:309-21. doi: 10.1007/82_2009_6.
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.
摘要
由于水痘带状疱疹病毒（VZV）是一种专门的人类病原体，因此需要开发动物模型来研究发病机制、潜伏期和再激活。非人类灵长类动物中猴水痘病毒（SVV）感染的病理、病毒学和免疫学特征与人类 VZV 感染相似。SVV 对食蟹猴和绿猴的自然感染以及 SVV 对恒河猴的支气管内接种均提供了最有用的模型来研究潜伏和宿主免疫反应的病毒和免疫学方面。对 SVV 潜伏感染的猴子进行实验性免疫抑制会导致带状疱疹，从而提供了一个新的模型系统来研究适应性免疫丧失如何调节病毒再激活。
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