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Molecular Mechanisms of Neurodegenerative Diseases Induced by Human Retroviruses: A Review

机译:人类逆转录病毒诱导的神经退行性疾病的分子机制:综述。

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Problem statement: Infection with retroviruses such as human immunodeficiency virus type 1 (HIV-1) and human T cell leukemia virus type 1 (HTLV-1) have been shown to lead to neurodegenerative diseases such as HIV-associated dementia (HAD) or neuroAIDS and HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP), respectively. Approach: HIV-1-induced neurologic disease is associated with an influx of HIV-infected monocytic cells across the blood-brain barrier. Following neuroinvasion, HIV-1 and viral proteins, in addition to cellular mediators released from infected and uninfected cells participate in astrocytic and neuronal dysregulation, leading to mild to severe neurocognitive disorders. Results: The molecular architecture of viral regulatory components including the Long Terminal Repeat (LTR), genes encoding the viral proteins Tat, Vpr and Nef as well as the envelope gene encoding gp120 and gp41 have been implicated in
机译:问题陈述:已证明感染逆转录病毒,例如人类免疫缺陷病毒1型(HIV-1)和人类T细胞白血病病毒1型(HTLV-1),可导致神经退行性疾病,例如HIV相关痴呆(HAD)或NeuroAIDS和HTLV-1相关性脊髓病/热带痉挛性轻瘫(HAM / TSP)。方法:HIV-1诱发的神经系统疾病与HIV感染的单核细胞跨过血脑屏障大量涌入有关。神经入侵后,除了感染和未感染细胞释放的细胞介体外,HIV-1和病毒蛋白还参与星形胶质细胞和神经元失调,导致轻度至重度神经认知障碍。结果:包括长末端重复序列(LTR),编码病毒蛋白Tat,Vpr和Nef的基因以及编码gp120和gp41的包膜基因在内的病毒调节成分的分子结构与

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