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首页> 外文期刊>Nature >The gene product Murr1 restricts HIV-1 replication in resting CD4~+ lymphocytes
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The gene product Murr1 restricts HIV-1 replication in resting CD4~+ lymphocytes

机译：基因产物Murr1限制HIV-1在静止的CD4〜+淋巴细胞中的复制

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摘要

Although human immunodeficiency virus-1 (HIV-1) infects quiescent and proliferating CD4~+ lymphocytes, the virus replicates poorly in resting T cells. Factors that block viral replication in these cells might help to prolong the asymptomatic phase of HIV infection; however, the molecular mechanisms that control this process are not fully understood. Here we show that Murr1, a gene product known previously for its involvement in copper regulation, inhibits HIV-1 growth in unstimulated CD4~+ T cells. This inhibition was mediated in part through its ability to inhibit basal and cytokine-stimulated nuclear factor (NF)-κB activity. Knockdown of Murr1 increased NF-κB activity and decreased IκB-α concentrations by facilitating phospho-IκB-α degradation by the proteasome. Murr1 was detected in CD4~+ T cells, and RNA-mediated interference of Murr1 in primary resting CD4~+ lymphocytes increased HIV-1 replication. Through its effects on the proteasome, Murr1 acts as a genetic restriction factor that inhibits HIV-1 replication in lymphocytes, which could contribute to the regulation of asymptomatic HIV infection and the progression of AIDS.
机译：尽管人类免疫缺陷病毒1（HIV-1）感染静止和增殖的CD4〜+淋巴细胞，但该病毒在静止的T细胞中复制能力很差。阻碍这些细胞中病毒复制的因素可能有助于延长HIV感染的无症状期。但是，控制该过程的分子机理尚未完全了解。在这里，我们表明，Murr1是一种以前因参与铜调节而闻名的基因产物，可抑制未刺激的CD4〜+ T细胞中的HIV-1生长。这种抑制作用部分是由于其抑制基础和细胞因子刺激的核因子（NF）-κB活性的能力而介导的。抑制Murr1可通过促进蛋白酶体降解磷酸化IκB-α而增加NF-κB活性并降低IκB-α浓度。在CD4〜+ T细胞中检测到Murr1，而RNA介导的Murr1对原代静息CD4〜+淋巴细胞的干扰增加了HIV-1复制。通过对蛋白酶体的作用，Murr1成为抑制淋巴细胞中HIV-1复制的遗传限制因子，这可能有助于调节无症状HIV感染和AIDS的发展。

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