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首页> 外文期刊>Retrovirology >Kaposi's sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-κB pathway and functionally cooperates with Tat
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Kaposi's sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-κB pathway and functionally cooperates with Tat

机译：卡波济氏肉瘤相关疱疹病毒编码的病毒FLICE抑制蛋白通过经典的NF-κB途径激活HIV-1长末端重复序列的转录并在功能上与Tat合作

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Background The nuclear transcription factor NF-κB binds to the HIV-1 long terminal repeat (LTR) and is a key regulator of HIV-1 gene expression in cells latently infected with this virus. In this report, we have analyzed the ability of Kaposi's sarcoma associate herpes virus (KSHV, also known as Human Herpes virus 8)-encoded viral FLIP (Fas-associated death domain-like IL-1 beta-converting enzyme inhibitory protein) K13 to activate the HIV-1 LTR. Results We present evidence that vFLIP K13 activates HIV-1 LTR via the activation of the classical NF-κB pathway involving c-Rel, p65 and p50 subunits. K13-induced HIV-1 LTR transcriptional activation requires the cooperative interaction of all three components of the IKK complex and can be effectively blocked by inhibitors of the classical NF-κB pathway. K13 mutants that lacked the ability to activate the NF-κB pathway also failed to activate the HIV-1 LTR. K13 could effectively activate a HIV-1 LTR reporter construct lacking the Tat binding site but failed to activate a construct lacking the NF-κB binding sites. However, coexpression of HIV-1 Tat with K13 led to synergistic activation of HIV-1 LTR. Finally, K13 differentially activated HIV-1 LTRs derived from different strains of HIV-1, which correlated with their responsiveness to NF-κB pathway. Conclusions Our results suggest that concomitant infection with KSHV/HHV8 may stimulate HIV-1 LTR via vFLIP K13-induced classical NF-κB pathway which cooperates with HIV-1 Tat protein.
机译：背景技术核转录因子NF-κB与HIV-1长末端重复序列（LTR）结合，并且是潜在感染该病毒的细胞中HIV-1基因表达的关键调节剂。在本报告中，我们分析了卡波西氏肉瘤相关疱疹病毒（KSHV，也称为人疱疹病毒8）编码的病毒FLIP（Fas相关死亡域样IL-1β转化酶抑制蛋白）K13的能力。激活HIV-1 LTR。结果我们提供的证据表明，vFLIP K13通过涉及c-Rel，p65和p50亚基的经典NF-κB途径激活HIV-1 LTR。 K13诱导的HIV-1 LTR转录激活需要IKK复合体的所有三个组件的协同相互作用，并且可以被经典NF-κB途径的抑制剂有效地阻断。缺乏激活NF-κB通路能力的K13突变体也未能激活HIV-1 LTR。 K13可以有效激活缺少Tat结合位点的HIV-1 LTR报告基因构建体，但不能激活缺少NF-κB结合位点的构建体。但是，HIV-1 Tat与K13的共表达导致HIV-1 LTR的协同激活。最后，K13差异激活了HIV-1 LTR，这些HIV-1 LTR来自不同的HIV-1毒株，这与其对NF-κB途径的反应性相关。结论我们的结果表明，伴随着KSHV / HHV8感染可通过vFLIP K13诱导的经典NF-κB途径与HIV-1 Tat蛋白协同作用来刺激HIV-1 LTR。

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