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首页> 外文期刊>AIDS Research and Human Retroviruses >Non-POU Domain-Containing Octamer-Binding Protein Negatively Regulates HIV-1 Infection in CD4(+) T Cells
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Non-POU Domain-Containing Octamer-Binding Protein Negatively Regulates HIV-1 Infection in CD4(+) T Cells

机译：非包含POU域的八聚体结合蛋白负面调节CD4（+）T细胞中的HIV-1感染。

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摘要

HIV-1 interacts with numerous cellular proteins during viral replication. Identifying such host proteins and characterizing their roles in HIV-1 infection can deepen our understanding of the dynamic interplay between host and pathogen. We previously identified non-POU domain-containing octamer-binding protein (NonO or p54nrb) as one of host factors associated with catalytically active preintegration complexes (PIC) of HIV-1 in infected CD4(+) T cells. NonO is involved in nuclear processes including transcriptional regulation and RNA splicing. Although NonO has been identified as an HIV-1 interactant in several recent studies, its role in HIV-1 replication has not been characterized. We investigated the effect of NonO on the HIV-1 life cycle in CD4(+) T cell lines and primary CD4(+) T cells using single-cycle and replication-competent HIV-1 infection assays. We observed that short hairpin RNA (shRNA)-mediated stable NonO knockdown in a CD4(+) Jurkat T cell line and primary CD4(+) T cells did not affect cell viability or proliferation, but enhanced HIV-1 infection. The enhancement of HIV-1 infection in Jurkat T cells correlated with increased viral reverse transcription and gene expression. Knockdown of NonO expression in Jurkat T cells modestly enhanced HIV-1 gag mRNA expression and Gag protein synthesis, suggesting that viral gene expression and RNA regulation are the predominantly affected events causing enhanced HIV-1 replication in NonO knockdown (KD) cells. Furthermore, overexpression of NonO in Jurkat T cells reduced HIV-1 single-cycle infection by 41% compared to control cells. Our data suggest that NonO negatively regulates HIV-1 infection in CD4(+) T cells, albeit it has modest effects on early and late stages of the viral life cycle, highlighting the importance of host proteins associated with HIV-1 PIC in regulating viral replication.
机译：在病毒复制过程中，HIV-1与许多细胞蛋白相互作用。鉴定此类宿主蛋白并表征其在HIV-1感染中的作用可以加深我们对宿主与病原体之间动态相互作用的理解。我们之前确定非含POU域的八聚体结合蛋白（NonO或p54nrb）是与感染CD4（+）T细胞中HIV-1的催化活性预整合复合物（PIC）相关的宿主因子之一。 NonO参与核过程，包括转录调控和RNA剪接。尽管在最近的几项研究中已将NonO鉴定为HIV-1相互作用物，但尚未鉴定其在HIV-1复制中的作用。我们使用单周期和具有复制能力的HIV-1感染试验研究了NonO对CD4（+）T细胞系和原代CD4（+）T细胞中HIV-1生命周期的影响。我们观察到，短发夹RNA（shRNA）介导的CD4（+）Jurkat T细胞系和原代CD4（+）T细胞中稳定的NonO敲除不会影响细胞活力或增殖，但会增强HIV-1感染。 Jurkat T细胞中HIV-1感染的增强与病毒逆转录和基因表达的增加有关。抑制Jurkat T细胞中NonO表达的表达可适度增强HIV-1 gag mRNA表达和Gag蛋白质的合成，这表明病毒基因表达和RNA调节是主要的事件，其导致Non-1基因敲除（KD）细胞中HIV-1复制的增强。此外，与对照细胞相比，Jurkat T细胞中NonO的过度表达将HIV-1单周期感染减少了41％。我们的数据表明，NonO负调节CD4（+）T细胞中的HIV-1感染，尽管它对病毒生命周期的早期和晚期具有适度的影响，突显了与HIV-1 PIC相关的宿主蛋白在调节病毒中的重要性复制。

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