Oglesbee Michael, Niewiesk Stefan
Department of Veterinary Biosciences, Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA.
Future Virol. 2011 Jan 1;6(1):85-99. doi: 10.2217/fvl.10.70.
Measles virus is highly neuroinvasive, yet host immune responses are highly effective at limiting neurovirulence in humans. We know that neurons are an important target of infection and that both IFN-γ and -β expression are observed in the measles virus-infected human brain. Rodent models can be used to understand how this response is orchestrated. Constitutive expression of the major inducible 70-kDa heat-shock protein is a feature of primate tissues that is lacking in mice. This article examines the importance of addressing this difference when modeling outcomes of brain infection in mice, particularly in terms of understanding how infected neurons may activate uninfected brain macrophages to produce IFN-β and support T-cell production of IFN-γ, a mediator of noncytolytic viral clearance. New and historical data suggest that the virus heat-shock protein 70 relationship is key to a protective host immune response and has potential broad relevance.
麻疹病毒具有高度神经侵袭性，但宿主免疫反应在限制人类神经毒力方面非常有效。我们知道神经元是感染的重要靶点，并且在感染麻疹病毒的人脑中观察到了IFN-γ和IFN-β的表达。啮齿动物模型可用于了解这种反应是如何协调的。主要诱导型70 kDa热休克蛋白的组成性表达是灵长类组织的一个特征，而小鼠缺乏这一特征。本文探讨了在小鼠大脑感染建模时解决这一差异的重要性，特别是在理解受感染神经元如何激活未感染的脑巨噬细胞以产生IFN-β并支持T细胞产生IFN-γ（一种非细胞溶解性病毒清除的介质）方面。新的和历史数据表明，病毒热休克蛋白70的关系是保护性宿主免疫反应的关键，并且具有潜在的广泛相关性。
