摘要
高活性抗逆转录病毒疗法 (HAART) 使感染1型人类免疫缺陷病毒(HIV-1)的患者寿命延长,生活质量大大提高。HAART疗法由各种干扰HIV-1生命周期各个阶段的药理抑制剂联合组成。然而,不间断的药物治疗往往导致寄主-病原关系的演变,从而导致耐药病毒株的出现。耐药HIV-1是一个巨大的威胁,因此,我们迫切需要寻求新的治疗分子。HIV-1使得CD4+/CD8+ T细胞耗竭并使患者细胞因子网络改变。肿瘤坏死因子α(TNF-alpha)是一种促炎性细胞因子,在HIV-1发病机制中有的十分重要的作用。HIV-1通过TNF-α信号通路扩大储存。某些HIV-1蛋白能模拟和调节TNF-α信号通路。TNF-alpha抑制剂在一定程度上已被用于某些炎症疾病。本文讨论了HIV-1发病机制中TNF-α的作用。此外,我们对TNF-α抑制剂治疗HIV-1感染进行了评估。
关键词: gp120,HAART, HIV-1,Nef,储存,Tat, TNF-alpha,Vpr。
图形摘要
Current Drug Targets
Title:Targeting TNF-Alpha in HIV-1 Infection
Volume: 17 Issue: 1
Author(s): Amit Kumar, Laurie Coquard and Georges Herbein
Affiliation:
关键词: gp120,HAART, HIV-1,Nef,储存,Tat, TNF-alpha,Vpr。
摘要: Highly active antiretroviral therapy (HAART) has dramatically extended the lifespan and quality of life of individuals infected with human immunodeficiency virus type 1 (HIV-1). HAART comprises of a cocktail of various pharmacological inhibitors which interfere with almost every stages of HIV-1 life cycle. However, constant application of drugs often results in the evolution of hostpathogen relationship resulting in the emergence of drug resistant viral strains. Drug resistant HIV-1 is a potent threat for the humankind. Therefore, there is a constant need to search for novel therapeutic molecules. HIV-1 infection results in the depletion of CD4+/CD8+T cells and alters the cytokine network in the infected individuals. Tumor necrosis factor alpha (TNF-alpha), a proinflammatory cytokine, plays a critical role in HIV-1 pathogenesis. HIV-1 utilizes the TNF-alpha signaling pathway for expanding its reservoir. Several HIV-1 proteins mimic and regulate the TNF-alpha signaling pathway. TNF-alpha inhibitors have been used in several inflammatory pathologies with success to some extent. In the present mini review we will discuss the role of TNF-alpha in HIV-1 pathogenesis. Furthermore we will evaluate the TNF-alpha inhibitors as an additional therapeutic option for HIV-1 infection.
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Cite this article as:
Amit Kumar, Laurie Coquard and Georges Herbein , Targeting TNF-Alpha in HIV-1 Infection, Current Drug Targets 2016; 17 (1) . https://dx.doi.org/10.2174/1573399811666150615145824
DOI https://dx.doi.org/10.2174/1573399811666150615145824 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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