• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

U1 和 OM10.1. 作为可逆转前病毒潜伏的替代模型的髓系细胞系。

U1 and OM10.1. Myeloid Cell Lines as Surrogate Models of Reversible Proviral Latency.

机构信息

Human Immuno-Virology (H.I.V.) Unit, San Raffaele Scientific Institute and School of Medicine, Vita-Salute San Raffaele University, Milano, Italy.

出版信息

Methods Mol Biol. 2022;2407:17-28. doi: 10.1007/978-1-0716-1871-4_2.

DOI:10.1007/978-1-0716-1871-4_2
PMID:34985654
Abstract

As already discussed for T cell lines, also myeloid cell lines as served as the earliest models of chronic HIV infection. They were particularly relevant in the late 1980s and early 1990s when most experimental in vitro infections were based on laboratory-adapted "T-cell tropic" strains of HIV-1, such as LAI/IIIB or others, that later were found to rely upon CXCR4 as coreceptor for viral entry in addition to CD4 as primary receptor. Although primary macrophages do express CXCR4 together with CD4, virus replication is much less efficient than that observed with CCR5-using "macrophage-tropic" strains, as discussed separately in this book. Although different myeloid cell lines have been used to generate models of chronic HIV-1 infection that could be used to investigate features of proviral reactivation, as reviewed in (Cassol et al. J Leukoc Biol 80:1018-1030, 2006), two cell lines in particular have been broadly used and will be here discussed: the U937-derived U1 and HL-60-derived OM-10.1.

摘要

正如前文讨论的 T 细胞系,髓系细胞系也被用作慢性 HIV 感染的最早模型。在 20 世纪 80 年代末和 90 年代初,当大多数体外实验感染都是基于实验室适应的“T 细胞嗜性”HIV-1 株,如 LAI/IIIB 或其他株时,它们尤其相关,后来发现这些株除了 CD4 作为主要受体外,还依赖 CXCR4 作为病毒进入的辅助受体。尽管原代巨噬细胞确实表达 CXCR4 和 CD4,但病毒复制的效率远低于使用 CCR5 的“巨噬细胞嗜性”株观察到的效率,这将在本书的其他部分单独讨论。尽管已经使用了不同的髓系细胞系来生成慢性 HIV-1 感染模型,这些模型可用于研究前病毒激活的特征,如(Cassol 等人,J Leukoc Biol 80:1018-1030, 2006)中所综述的,但有两种细胞系被广泛使用,这里将讨论:U937 衍生的 U1 和 HL-60 衍生的 OM-10.1。

相似文献

1
U1 and OM10.1. Myeloid Cell Lines as Surrogate Models of Reversible Proviral Latency.U1 和 OM10.1. 作为可逆转前病毒潜伏的替代模型的髓系细胞系。
Methods Mol Biol. 2022;2407:17-28. doi: 10.1007/978-1-0716-1871-4_2.
2
CD4 is expressed on a heterogeneous subset of hematopoietic progenitors, which persistently harbor CXCR4 and CCR5-tropic HIV proviral genomes in vivo.CD4在造血祖细胞的一个异质性亚群上表达,这些造血祖细胞在体内持续携带嗜CXCR4和CCR5的HIV前病毒基因组。
PLoS Pathog. 2017 Jul 21;13(7):e1006509. doi: 10.1371/journal.ppat.1006509. eCollection 2017 Jul.
3
Chemokine receptor-usage of clinical HIV-1 isolates obtained from patients with HIV-1 infection in late clinical stages using PHA-blast.使用PHA-母细胞从临床晚期HIV-1感染患者中获得的临床HIV-1分离株的趋化因子受体使用情况
Microbiol Immunol. 1999;43(10):967-74. doi: 10.1111/j.1348-0421.1999.tb03357.x.
4
Tat protein induces human immunodeficiency virus type 1 (HIV-1) coreceptors and promotes infection with both macrophage-tropic and T-lymphotropic HIV-1 strains.Tat蛋白可诱导1型人类免疫缺陷病毒(HIV-1)共受体,并促进巨噬细胞嗜性和T淋巴细胞嗜性HIV-1毒株的感染。
J Virol. 1998 Nov;72(11):8952-60. doi: 10.1128/JVI.72.11.8952-8960.1998.
5
Promonocytic U937 subclones expressing CD4 and CXCR4 are resistant to infection with and cell-to-cell fusion by T-cell-tropic human immunodeficiency virus type 1.表达CD4和CXCR4的单核细胞U937亚克隆对嗜T细胞性1型人类免疫缺陷病毒的感染及细胞间融合具有抗性。
J Virol. 1997 Dec;71(12):9664-71. doi: 10.1128/JVI.71.12.9664-9671.1997.
6
Coreceptor competition for association with CD4 may change the susceptibility of human cells to infection with T-tropic and macrophagetropic isolates of human immunodeficiency virus type 1.与CD4结合的共受体竞争可能会改变人类细胞对1型人类免疫缺陷病毒的T嗜性和巨噬细胞嗜性分离株感染的易感性。
J Virol. 2000 Jun;74(11):5016-23. doi: 10.1128/jvi.74.11.5016-5023.2000.
7
Role of CXCR4 in cell-cell fusion and infection of monocyte-derived macrophages by primary human immunodeficiency virus type 1 (HIV-1) strains: two distinct mechanisms of HIV-1 dual tropism.CXCR4在原代人类免疫缺陷病毒1型(HIV-1)毒株介导的单核细胞衍生巨噬细胞的细胞间融合及感染中的作用:HIV-1双嗜性的两种不同机制
J Virol. 1999 Sep;73(9):7117-25. doi: 10.1128/JVI.73.9.7117-7125.1999.
8
Concordant utilization of macrophage entry coreceptors by related variants within an HIV type 1 primary isolate viral swarm.HIV-1 原发性分离株病毒群体内相关变异体对巨噬细胞进入共受体的协同利用
AIDS Res Hum Retroviruses. 2001 Jul 1;17(10):957-63. doi: 10.1089/088922201750290078.
9
Alternative coreceptor requirements for efficient CCR5- and CXCR4-mediated HIV-1 entry into macrophages.替代核心受体对 CCR5 和 CXCR4 介导的 HIV-1 进入巨噬细胞的高效需求。
J Virol. 2011 Oct;85(20):10699-709. doi: 10.1128/JVI.05510-11. Epub 2011 Aug 10.
10
Primary human immunodeficiency virus type 2 (HIV-2) isolates infect CD4-negative cells via CCR5 and CXCR4: comparison with HIV-1 and simian immunodeficiency virus and relevance to cell tropism in vivo.原发性人类免疫缺陷病毒2型(HIV-2)分离株通过CCR5和CXCR4感染CD4阴性细胞:与HIV-1和猴免疫缺陷病毒的比较以及与体内细胞嗜性的相关性。
J Virol. 1999 Sep;73(9):7795-804. doi: 10.1128/JVI.73.9.7795-7804.1999.

引用本文的文献

1
SARS-CoV-2 Modulation of HIV Latency Reversal in a Myeloid Cell Line: Direct and Bystander Effects.SARS-CoV-2 对髓系细胞系中 HIV 潜伏期逆转的调节:直接和旁观者效应。
Viruses. 2024 Aug 17;16(8):1310. doi: 10.3390/v16081310.
2
Methamphetamine Induces the Release of Proadhesive Extracellular Vesicles and Promotes Syncytia Formation: A Potential Role in HIV-1 Neuropathogenesis.甲基苯丙胺诱导促黏附细胞外囊泡的释放并促进合胞体的形成:在 HIV-1 神经发病机制中的潜在作用。
Viruses. 2022 Mar 7;14(3):550. doi: 10.3390/v14030550.

本文引用的文献

1
Induction of E. coli-derived endonuclease MazF suppresses HIV-1 production and causes apoptosis in latently infected cells.诱导大肠杆菌来源的内切酶 MazF 可抑制 HIV-1 的产生并诱导潜伏感染细胞凋亡。
Biochem Biophys Res Commun. 2020 Sep 24;530(3):597-602. doi: 10.1016/j.bbrc.2020.07.103. Epub 2020 Aug 1.
2
Epigenetic Suppression of HIV in Myeloid Cells by the BRD4-Selective Small Molecule Modulator ZL0580.BRD4 选择性小分子调节剂 ZL0580 对髓样细胞中 HIV 的表观遗传抑制作用。
J Virol. 2020 May 18;94(11). doi: 10.1128/JVI.01880-19.
3
Transcriptional profiling indicates cAMP-driven reversal of HIV latency in monocytes occurs via transcription factor SP-1.
转录谱分析表明,cAMP 驱动的单核细胞中 HIV 潜伏期的逆转是通过转录因子 SP-1 发生的。
Virology. 2020 Mar;542:40-53. doi: 10.1016/j.virol.2020.01.006. Epub 2020 Jan 18.
4
Morphine Withdrawal Enhances HIV Infection of Macrophages.吗啡戒断增强巨噬细胞感染 HIV。
Front Immunol. 2019 Nov 15;10:2601. doi: 10.3389/fimmu.2019.02601. eCollection 2019.
5
Galectin-3 is involved in HIV-1 expression through NF-κB activation and associated with Tat in latently infected cells.半乳糖凝集素-3 通过 NF-κB 激活参与 HIV-1 表达,并与潜伏感染细胞中的 Tat 相关。
Virus Res. 2019 Jan 15;260:86-93. doi: 10.1016/j.virusres.2018.11.012. Epub 2018 Nov 24.
6
Mesenchymal stem cells are attracted to latent HIV-1-infected cells and enable virus reactivation via a non-canonical PI3K-NFκB signaling pathway.间充质干细胞被潜伏感染 HIV-1 的细胞吸引,并通过非经典的 PI3K-NFκB 信号通路促进病毒激活。
Sci Rep. 2018 Oct 2;8(1):14702. doi: 10.1038/s41598-018-32657-y.
7
TSC1 and DEPDC5 regulate HIV-1 latency through the mTOR signaling pathway.TSC1 和 DEPDC5 通过 mTOR 信号通路调节 HIV-1 潜伏期。
Emerg Microbes Infect. 2018 Aug 8;7(1):138. doi: 10.1038/s41426-018-0139-5.
8
BI-2536 and BI-6727, dual Polo-like kinase/bromodomain inhibitors, effectively reactivate latent HIV-1.BI-2536 和 BI-6727 是双重 Polo 样激酶/溴结构域抑制剂,能有效重新激活潜伏的 HIV-1。
Sci Rep. 2018 Feb 23;8(1):3521. doi: 10.1038/s41598-018-21942-5.
9
HIV integration sites in latently infected cell lines: evidence of ongoing replication.潜伏感染细胞系中的HIV整合位点:持续复制的证据。
Retrovirology. 2017 Jan 13;14(1):2. doi: 10.1186/s12977-016-0325-2.
10
Differences in Activation of HIV-1 Replication by Superinfection With HIV-1 and HIV-2 in U1 Cells.U1细胞中HIV-1和HIV-2双重感染对HIV-1复制激活的差异
J Cell Physiol. 2017 Jul;232(7):1746-1753. doi: 10.1002/jcp.25614. Epub 2016 Sep 30.