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HIV-Associated Neurotoxicity: The Interplay of Host and Viral Proteins
Mediators of Inflammation ( IF 4.4 ) Pub Date : 2021-08-25 , DOI: 10.1155/2021/1267041
Sushama Jadhav 1, 2 , Vijay Nema 1
Affiliation  

HIV-1 can incite activation of chemokine receptors, inflammatory mediators, and glutamate receptor-mediated excitotoxicity. The mechanisms associated with such immune activation can disrupt neuronal and glial functions. HIV-associated neurocognitive disorder (HAND) is being observed since the beginning of the AIDS epidemic due to a change in the functional integrity of cells from the central nervous system (CNS). Even with the presence of antiretroviral therapy, there is a decline in the functioning of the brain especially movement skills, noticeable swings in mood, and routine performance activities. Under the umbrella of HAND, various symptomatic and asymptomatic conditions are categorized and are on a rise despite the use of newer antiretroviral agents. Due to the use of long-lasting antiretroviral agents, this deadly disease is becoming a manageable chronic condition with the occurrence of asymptomatic neurocognitive impairment (ANI), symptomatic mild neurocognitive disorder, or HIV-associated dementia. In-depth research in the pathogenesis of HIV has focused on various mechanisms involved in neuronal dysfunction and associated toxicities ultimately showcasing the involvement of various pathways. Increasing evidence-based studies have emphasized a need to focus and explore the specific pathways in inflammation-associated neurodegenerative disorders. In the current review, we have highlighted the association of various HIV proteins and neuronal cells with their involvement in various pathways responsible for the development of neurotoxicity.

中文翻译:

HIV 相关的神经毒性:宿主和病毒蛋白的相互作用

HIV-1 可以激发趋化因子受体、炎症介质和谷氨酸受体介导的兴奋性毒性的激活。与这种免疫激活相关的机制可以破坏神经元和神经胶质细胞的功能。自 AIDS 流行开始以来,由于中枢神经系统 (CNS) 细胞的功能完整性发生变化,人们就观察到 HIV 相关的神经认知障碍 (HAND)。即使存在抗逆转录病毒疗法,大脑功能也会下降,尤其是运动技能、情绪明显波动和日常表演活动。在 HAND 的保护伞下,尽管使用了较新的抗逆转录病毒药物,但对各种有症状和无症状的疾病进行了分类并且呈上升趋势。由于使用长效抗逆转录病毒药物,随着无症状神经认知障碍 (ANI)、有症状的轻度神经认知障碍或 HIV 相关性痴呆的发生,这种致命的疾病正在成为一种可控制的慢性病。对 HIV 发病机制的深入研究集中在与神经元功能障碍和相关毒性有关的各种机制上,最终展示了各种途径的参与。越来越多的循证研究强调需要关注和探索炎症相关神经退行性疾病的特定途径。在当前的审查中,我们强调了各种 HIV 蛋白和神经元细胞与它们参与导致神经毒性发展的各种途径的关联。有症状的轻度神经认知障碍或 HIV 相关性痴呆。对 HIV 发病机制的深入研究集中在与神经元功能障碍和相关毒性有关的各种机制上,最终展示了各种途径的参与。越来越多的循证研究强调需要关注和探索炎症相关神经退行性疾病的特定途径。在当前的审查中,我们强调了各种 HIV 蛋白和神经元细胞与它们参与导致神经毒性发展的各种途径的关联。有症状的轻度神经认知障碍或 HIV 相关性痴呆。对 HIV 发病机制的深入研究集中在与神经元功能障碍和相关毒性有关的各种机制上,最终展示了各种途径的参与。越来越多的循证研究强调需要关注和探索炎症相关神经退行性疾病的特定途径。在当前的审查中,我们强调了各种 HIV 蛋白和神经元细胞与它们参与导致神经毒性发展的各种途径的关联。对 HIV 发病机制的深入研究集中在与神经元功能障碍和相关毒性有关的各种机制上,最终展示了各种途径的参与。越来越多的循证研究强调需要关注和探索炎症相关神经退行性疾病的特定途径。在当前的审查中,我们强调了各种 HIV 蛋白和神经元细胞与它们参与导致神经毒性发展的各种途径的关联。对 HIV 发病机制的深入研究集中在与神经元功能障碍和相关毒性有关的各种机制上,最终展示了各种途径的参与。越来越多的循证研究强调需要关注和探索炎症相关神经退行性疾病的特定途径。在当前的审查中,我们强调了各种 HIV 蛋白和神经元细胞与它们参与导致神经毒性发展的各种途径的关联。
更新日期:2021-08-25
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