T-Cell Signaling in HIV-1 Infection.

The Open Virology Journal Pub Date : 2013-07-26 eCollection Date: 2013-01-01 DOI:10.2174/1874357920130621001
Wasim Abbas, Georges Herbein
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引用次数: 31

Abstract

HIV exploits the T-cell signaling network to gain access to downstream cellular components, which serves as effective tools to break the cellular barriers. Multiple host factors and their interaction with viral proteins contribute to the complexity of HIV-1 pathogenesis and disease progression. HIV-1 proteins gp120, Nef, Tat and Vpr alter the T-cell signaling pathways by activating multiple transcription factors including NF-ĸB, Sp1 and AP-1. HIV-1 evades the immune system by developing a multi-pronged strategy. Additionally, HIV-1 encoded proteins influence the apoptosis in the host cell favoring or blocking T-cell apoptosis. Thus, T-cell signaling hijacked by viral proteins accounts for both viral persistence and immune suppression during HIV-1 infection. Here, we summarize past and present studies on HIV-1 T-cell signaling with special focus on the possible role of T cells in facilitating viral infection and pathogenesis.

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HIV-1感染中的t细胞信号传导
HIV利用t细胞信号网络进入下游细胞成分,这是打破细胞屏障的有效工具。多种宿主因子及其与病毒蛋白的相互作用导致了HIV-1发病机制和疾病进展的复杂性。HIV-1蛋白gp120、Nef、Tat和Vpr通过激活包括NF-ĸB、Sp1和AP-1在内的多种转录因子来改变t细胞信号通路。HIV-1通过发展多管齐下的策略来逃避免疫系统。此外,HIV-1编码的蛋白影响宿主细胞的凋亡,有利于或阻断t细胞凋亡。因此,被病毒蛋白劫持的t细胞信号解释了HIV-1感染期间病毒的持久性和免疫抑制。在这里,我们总结了过去和现在关于HIV-1 T细胞信号传导的研究,特别关注T细胞在促进病毒感染和发病机制中的可能作用。
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