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2
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本文引用的文献

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Actin-dependent receptor colocalization required for human immunodeficiency virus entry into host cells.人类免疫缺陷病毒进入宿主细胞所需的肌动蛋白依赖性受体共定位。
J Virol. 1998 Jun;72(6):5251-5. doi: 10.1128/JVI.72.6.5251-5255.1998.
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Aminooxypentane-RANTES induces CCR5 internalization but inhibits recycling: a novel inhibitory mechanism of HIV infectivity.氨氧基戊烷-调节激活正常T细胞表达和分泌因子(RANTES)诱导CCR5内化但抑制再循环:一种新的HIV感染抑制机制
J Exp Med. 1998 Apr 20;187(8):1215-24. doi: 10.1084/jem.187.8.1215.
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Dichotomous effects of beta-chemokines on HIV replication in monocytes and monocyte-derived macrophages.β趋化因子对单核细胞及单核细胞衍生巨噬细胞中HIV复制的二分效应。
J Immunol. 1998 Apr 1;160(7):3091-5.
4
Increased replication of T-cell-tropic HIV strains and CXC-chemokine receptor-4 induction in T cells treated with macrophage inflammatory protein (MIP)-1alpha, MIP-1beta and RANTES beta-chemokines.在用巨噬细胞炎性蛋白(MIP)-1α、MIP-1β和调节激活正常T细胞表达和分泌因子(RANTES)β趋化因子处理的T细胞中,嗜T细胞性HIV毒株的复制增加以及CXC趋化因子受体4的诱导。
AIDS. 1998 Jan 22;12(2):183-90. doi: 10.1097/00002030-199802000-00008.
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HIV type 1 V3 variation dynamics in vivo: long-term persistence of non-syncytium-inducing genotypes and transient presence of syncytium-inducing genotypes during the course of progressive AIDS.1型人类免疫缺陷病毒(HIV-1)V3区体内变异动态:非合胞体诱导基因型的长期持续存在以及在进行性艾滋病病程中合胞体诱导基因型的短暂出现。
AIDS Res Hum Retroviruses. 1997 Dec 10;13(18):1597-609. doi: 10.1089/aid.1997.13.1597.
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HIV-1 gp120 induces an association between CD4 and the chemokine receptor CXCR4.人类免疫缺陷病毒1型糖蛋白120(HIV-1 gp120)诱导CD4与趋化因子受体CXCR4之间产生关联。
J Immunol. 1997 Sep 15;159(6):3000-8.
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Polarization of chemokine receptors to the leading edge during lymphocyte chemotaxis.淋巴细胞趋化作用过程中趋化因子受体向前沿的极化。
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Potent inhibition of HIV-1 infectivity in macrophages and lymphocytes by a novel CCR5 antagonist.一种新型CCR5拮抗剂对巨噬细胞和淋巴细胞中HIV-1感染性的强效抑制作用。
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Evolutionary mechanisms and population dynamics of the third variable envelope region of HIV within single hosts.单一宿主内HIV第三个可变包膜区域的进化机制与种群动态
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10
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CC趋化因子增强HIV-1 T嗜性毒株在CD4(+) T细胞中的复制:信号转导的作用

CC-chemokines enhance the replication of T-tropic strains of HIV-1 in CD4(+) T cells: role of signal transduction.

作者信息

Kinter A, Catanzaro A, Monaco J, Ruiz M, Justement J, Moir S, Arthos J, Oliva A, Ehler L, Mizell S, Jackson R, Ostrowski M, Hoxie J, Offord R, Fauci A S

机构信息

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11880-5. doi: 10.1073/pnas.95.20.11880.

DOI:10.1073/pnas.95.20.11880
PMID:9751759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC21734/
Abstract

This study demonstrates that several CC-chemokines, including those that inhibit entry and replication of macrophage-tropic strains of HIV, increase the replication of T cell (T)-tropic strains in CD4(+) T cells. Enhancement of T-tropic HIV replication is observed at early stages of replication, requires signaling through inhibitory guanine nucleotide-binding regulatory (Gi) proteins, and is associated with increased cell surface colocalization of CD4 and the T-tropic HIV coreceptor CXCR4. These findings may further our understanding of the factors that influence the replication and spread of T-tropic strains of HIV in vivo and suggest that the use of cell signaling CC-chemokines as therapeutic agents for the purpose of limiting HIV replication in vivo should be approached with caution.

摘要

本研究表明,几种CC趋化因子,包括那些抑制HIV巨噬细胞嗜性毒株进入和复制的趋化因子,可增加CD4(+)T细胞中T细胞嗜性毒株的复制。在复制早期即可观察到T嗜性HIV复制增强,这需要通过抑制性鸟嘌呤核苷酸结合调节(Gi)蛋白进行信号传导,并且与CD4和T嗜性HIV共受体CXCR4在细胞表面的共定位增加有关。这些发现可能会加深我们对影响HIV T嗜性毒株在体内复制和传播因素的理解,并表明将细胞信号CC趋化因子用作体内限制HIV复制的治疗药物时应谨慎行事。