摘要
Nef是只在灵长类动物慢病毒中表达的一种辅助蛋白。它作为一种接合/支架蛋白,在与细胞蛋白相互作用的时,是没有酶活性的。Nef的细胞内功能在很大程度上能够解释许多AIDS 病的致病作用。尽管缺乏已知的分泌途径,但我们可以检测出HIV-1感染患者血浆中Nef 5-10 ng/ml的浓度变化。值得注意的是,AIDS患者血浆中Nef蛋白水平与病毒载量和CD4 + T淋巴细胞的数量无关,即使进行抗逆转录病毒治疗也是如此。本文对Nef如何从 HIV-1感染细胞转移至旁边细胞以及在不同类型细胞的胞外Nef的影响进行了概括总结。总之,大量实验证明,Nef在艾滋病的发病机制中起重要作用。因此,对Nef抑制药物的识别研究将有助于在目前抗逆转录病毒疗法基础上建立新的治疗方法。
关键词: ADAM17,细胞信号转导,外泌体,HIV-1感染,纳米管,Nef。
图形摘要
Current Drug Targets
Title:The Contribution of Extracellular Nef to HIV-Induced Pathogenesis
Volume: 17 Issue: 1
Author(s): Eleonora Olivetta, Claudia Arenaccio, Francesco Manfredi, Simona Anticoli and Maurizio Federico
Affiliation:
关键词: ADAM17,细胞信号转导,外泌体,HIV-1感染,纳米管,Nef。
摘要: Nef is an accessory protein expressed exclusively in primate lentiviruses. It is devoid of enzymatic activities while interacting with several cell proteins as an adaptor/scaffold protein. Intracellular functions of Nef largely account for many pathogenic effects observed in AIDS disease. Nef, despite lacking known secretory pathways, can be detected in plasma of HIV-1-infected patients at the concentration varing from 5 to 10 ng/ml. Remarkably, the levels of Nef in plasma of HIV patients do not correlate with viral load or number of CD4+ T lymphocytes, and persist during antiretroviral therapy. Here, we review literature data describing how Nef can be transmitted from HIV-1- infected cells to bystander ones, and the effects of extracellular Nef in different cell types. Overall, large part of experimental evidences supports the idea that extracellular Nef plays a relevant role in AIDS pathogenesis. Hence, efforts focused on the identification of Nef-inhibiting drugs would be of relevance to establish new therapeutic approaches supporting current antiretroviral therapies.
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Cite this article as:
Eleonora Olivetta, Claudia Arenaccio, Francesco Manfredi, Simona Anticoli and Maurizio Federico , The Contribution of Extracellular Nef to HIV-Induced Pathogenesis, Current Drug Targets 2016; 17 (1) . https://dx.doi.org/10.2174/1389450116666151001110126
DOI https://dx.doi.org/10.2174/1389450116666151001110126 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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