Gold L H, Fox H S, Henriksen S J, Buchmeier M J, Weed M R, Taffe M A, Huitrón-Resendiz S, Horn T F, Bloom F E
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.
J Med Primatol. 1998 Apr-Jun;27(2-3):104-12. doi: 10.1111/j.1600-0684.1998.tb00234.x.
A model is proposed in which a neurovirulent, microglial-passaged, simian immunodeficiency virus (SIV) is used to produce central nervous system (CNS) pathology and behavioral deficits in rhesus monkeys reminiscent of those seen in humans infected with human immunodeficiency virus (HIV). The time course of disease progression was characterized by using functional measures of cognition and motor skill, as well as neurophysiologic monitoring. Concomitant assessment of immunological and virological parameters illustrated correspondence between impaired behavioral performance and viral pathogenesis. Convergent results were obtained from neuropathological findings indicative of significant CNS disease. In ongoing studies, this SIV model is being used to explore the behavioral sequelae of immunodeficiency virus infection, the viral and host factors leading to neurologic dysfunction, and to begin testing potential therapeutic agents.
提出了一种模型，其中使用一种具有神经毒性、经小胶质细胞传代的猿猴免疫缺陷病毒（SIV），在恒河猴中产生中枢神经系统（CNS）病变和行为缺陷，这些病变和缺陷使人联想到感染人类免疫缺陷病毒（HIV）的人类所出现的情况。通过使用认知和运动技能的功能测量以及神经生理学监测来表征疾病进展的时间进程。免疫和病毒学参数的同步评估表明行为表现受损与病毒发病机制之间存在对应关系。从表明存在严重中枢神经系统疾病的神经病理学发现中获得了趋同的结果。在正在进行的研究中，这种SIV模型正被用于探索免疫缺陷病毒感染的行为后遗症、导致神经功能障碍的病毒和宿主因素，并开始测试潜在的治疗药物。
