Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism.

Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism.
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DOI:
10.3390/v10080409
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发表时间:
2018-08-04
期刊:
Viruses
影响因子:
--
通讯作者:
Chen X
Chen X
中科院分区:
其他
文献类型:
--
作者:
Deng L;Zeng Q;Wang M;Cheng A;Jia R;Chen S;Zhu D;Liu M;Yang Q;Wu Y;Zhao X;Zhang S;Liu Y;Yu Y;Zhang L;Chen X

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核因子-κB(NF-κB)是一种重要的转录因子,可诱导抗病毒基因和病毒基因的表达。NF-κB激活需要NF-κB上游分子的激活,包括受体、衔接蛋白、NF-κB(IκB)激酶(IKK)、IκBα和NF-κB二聚体p50/p65。为了生存,病毒已经进化出利用各种抑制NF-κB活性的策略的能力,包括靶向受体、衔接蛋白、IKK、IκBα和p50/p65。为了抑制NF-κB活化,病毒编码几种特异性NF-κB抑制剂,包括NS 3/4、3C和3C样蛋白酶、病毒去泛素化酶(DUB)、磷酸化蛋白样(PDL)基序、病毒蛋白磷酸酶(PPase)结合蛋白和小疏水(SH)蛋白。最后,我们简要描述了人类免疫缺陷病毒1型(HIV-1)通过抑制NF-κB活性在生产性和潜伏性感染中的免疫逃避机制。本文就NF-κB活化抑制在病毒免疫逃逸中的作用机制进行综述,以期为病毒性疾病的防治提供新的思路和参考。
Nuclear factor-κB (NF-κB) is an important transcription factor that induces the expression of antiviral genes and viral genes. NF-κB activation needs the activation of NF-κB upstream molecules, which include receptors, adaptor proteins, NF-κB (IκB) kinases (IKKs), IκBα, and NF-κB dimer p50/p65. To survive, viruses have evolved the capacity to utilize various strategies that inhibit NF-κB activity, including targeting receptors, adaptor proteins, IKKs, IκBα, and p50/p65. To inhibit NF-κB activation, viruses encode several specific NF-κB inhibitors, including NS3/4, 3C and 3C-like proteases, viral deubiquitinating enzymes (DUBs), phosphodegron-like (PDL) motifs, viral protein phosphatase (PPase)-binding proteins, and small hydrophobic (SH) proteins. Finally, we briefly describe the immune evasion mechanism of human immunodeficiency virus 1 (HIV-1) by inhibiting NF-κB activity in productive and latent infections. This paper reviews a viral mechanism of immune evasion that involves the suppression of NF-κB activation to provide new insights into and references for the control and prevention of viral diseases.
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