Sharer L R, Baskin G B, Cho E S, Murphey-Corb M, Blumberg B M, Epstein L G
Department of Pathology, UMD-New Jersey Medical School, Newark 07103.
Ann Neurol. 1988;23 Suppl:S108-12. doi: 10.1002/ana.410230727.
The simian immunodeficiency virus (SIV) is closely related to the human immunodeficiency virus (HIV) in genomic organization and morphology. More important, SIV and HIV are both primate lentiviruses that cause transmissible immunodeficiency and encephalitis, with an apparently increased virulence in the immature host. The neuropathological features in common between SIV encephalitis in juvenile macaque monkeys and HIV encephalitis in children include the invasion of brain with virus-laden macrophages, the formation of multinucleated (syncytial) giant cells, and white matter lesions and subtle white matter astrocytosis. Important differences include giant cell leptomeningitis and evidence of necrosis and karyorrhexis in brain macrophage infiltrates in SIV-infected monkeys. These changes probably represent a more acute inflammatory process. The importance of future studies to define pathogenetic features of SIV encephalitis, using molecularly characterized isolates with varying neurovirulence and host range, are emphasized.
猿猴免疫缺陷病毒（SIV）在基因组结构和形态上与人类免疫缺陷病毒（HIV）密切相关。更重要的是，SIV和HIV都是灵长类慢病毒，可导致可传播的免疫缺陷和脑炎，在未成熟宿主中其毒力明显增强。幼年猕猴的SIV脑炎和儿童的HIV脑炎共有的神经病理学特征包括载有病毒的巨噬细胞侵入大脑、多核（合胞体）巨细胞的形成、白质病变以及轻微的白质星形细胞增多。重要的差异包括巨细胞软脑膜炎以及SIV感染猴子大脑巨噬细胞浸润中的坏死和核碎裂证据。这些变化可能代表了一个更急性的炎症过程。强调了未来研究利用具有不同神经毒力和宿主范围的分子特征分离株来确定SIV脑炎致病特征的重要性。
