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首页> 外文期刊>Cytokine >Regulation of HIV-1 latency by T-cell activation.
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Regulation of HIV-1 latency by T-cell activation.

机译：通过T细胞活化来调节HIV-1潜伏期。

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摘要

HIV-infected patients harbor approximately 10(5)-10(6) memory CD4 T-cells that contain fully integrated but transcriptionally silent HIV proviruses. While small in number, these latently infected cells form a drug-insensitive reservoir that importantly contributes to the life-long persistence of HIV despite highly effective antiviral therapy. In tissue culture, latent HIV proviruses can be activated when their cellular hosts are exposed to select proinflammatory cytokines or their T-cell receptors are ligated. However, due to a lack of potency and/or dose-limiting toxicity, attempts to purge virus from this latent reservoir in vivo with immune-activating agents, such as anti-CD3 antibodies and IL-2, have failed. A deeper understanding of the molecular underpinnings of HIV latency is clearly required, including determining whether viral latency is actively reinforced by transcriptional repressors, defining which inducible host transcription factors most effectively antagonize latency, and elucidating the role of chromatin in viral latency. Only through such an improved understanding will it be possible to identify combination therapies that might allow complete purging of the latent reservoir and to realize the difficult and elusive goal of complete eradication of HIV in infected patients.
机译：被HIV感染的患者带有大约10（5）-10（6）个记忆CD4 T细胞，其中包含完全整合但转录沉默的HIV前病毒。这些潜伏感染的细胞虽然数量很少，但却形成了对药物不敏感的储库，尽管进行了有效的抗病毒治疗，但仍可为HIV的终身持续生存做出重要贡献。在组织培养中，潜在的HIV原病毒可以在其细胞宿主暴露于选择的促炎细胞因子或连接其T细胞受体时被激活。然而，由于缺乏效力和/或剂量限制的毒性，尝试用诸如抗CD3抗体和IL-2之类的免疫激活剂在体内从该潜伏的贮库中清除病毒的尝试失败了。显然需要对HIV潜伏期的分子基础有更深入的了解，包括确定转录抑制因子是否能有效地增强病毒潜伏期，定义哪些诱导型宿主转录因子最有效地拮抗潜伏期，以及阐明染色质在病毒潜伏期中的作用。只有通过这种更好的理解，才有可能确定可能允许彻底清除潜伏储库的联合疗法，并实现在感染患者中彻底根除艾滋病毒这一艰巨而难以实现的目标。

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