Nonhuman primate models of NeuroAIDS.
Nonhuman primate models of NeuroAIDS.
复制标题
神经辅助的非人类灵长类动物模型。
DOI：
10.1080/13550280802074539
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发表时间：
2008-08
影响因子：
3.2
通讯作者：
Buch S
中科院分区：
文献类型：
--
作者：
Williams R;Bokhari S;Silverstein P;Pinson D;Kumar A;Buch S
引起获得性免疫缺陷综合征（艾滋病）的人类免疫缺陷病毒（HIV）也表现为神经系统并发症。hiv相关痴呆（HAD）是hiv诱导的最严重的神经认知障碍。HIV脑炎（HIVE）是HAD的病理相关，其特征是形成多核巨细胞和小胶质结节，星形细胞增多，神经元损伤和丢失。对人类HAD疾病进展的病理评估是不可能的，唯一收集到的数据来自于已经屈服于这种疾病的个体，充其量是对终末期疾病的短暂了解。因此，相关的动物模型已经被开发出来，以缓解神经病毒学和神经炎症领域的知识差距。一般来说，最广泛使用的动物模型是猴免疫缺陷病毒（SIV）和嵌合猴/人免疫缺陷病毒（SHIV）猕猴模型系统。尽管SIV和SHIV模型系统都能够增强神经侵袭和伴随的神经病理学，类似于在人类综合征中看到的，但两者在疾病发病机制和进展方面的先天差异使得两个独立但有效的系统用于研究hiv相关神经病理学。
Human Immunodeficiency virus (HIV), the virus that causes acquired immunodeficiency syndrome (AIDS), also manifests neurological complications. HIV-associated dementia (HAD) is the most severe form of HIV-induced neurocognitive disorders. HIV encephalitis (HIVE), the pathological correlate of HAD, is characterized by the formation of multinucleated giant cells and microglial nodules, astrocytosis, and neuronal damage and loss. Pathological evaluation of HAD disease progression in humans is not possible, with the only data collected being from individuals who have succumbed to the disorder, a snap shot of end-stage disease at best. Therefore, pertinent animal models have been developed to alleviate this gap of knowledge in the field of neurovirology and neuroinflammation. In general, the most widely used animal models are the simian immunodeficiency virus (SIV) and the chimeric simian/human immunodeficiency virus (SHIV) macaque model systems. Although both SIV and SHIV model systems are able to potentiate neuroinvasion and the concomitant neuropathology similar to that seen in the human syndromes, the innate differences between the two in disease pathogenesis and progression make for two separate, yet effective, systems for the study of HIV-associated neuropathology.
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影响因子：
1.5
作者：
Joag, SV;Li, ZA;Narayan, O
通讯作者：
Narayan, O
影响因子：
5.4
作者：
Joag, SV;Li, Z;Narayan, O
通讯作者：
Narayan, O
影响因子：
56.9
作者：
Harouse, JM;Gettie, A;Cheng-Mayer, C
通讯作者：
Cheng-Mayer, C
影响因子：
120.7
作者：
CLERICI, M;LEVIN, JM;SHEARER, GM
通讯作者：
SHEARER, GM
影响因子：
5.4
作者：
Harouse, JM;Gettie, A;Cheng-Mayer, C
通讯作者：
Cheng-Mayer, C