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JCI Insight. 2020 Oct 15;5(20):139783. doi: 10.1172/jci.insight.139783.
2
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Retrovirology. 2019 Nov 11;16(1):32. doi: 10.1186/s12977-019-0494-x.
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Redefine statistical significance.重新定义统计学显著性。
Nat Hum Behav. 2018 Jan;2(1):6-10. doi: 10.1038/s41562-017-0189-z.
4
Entry of Polarized Effector Cells into Quiescence Forces HIV Latency.极化效应细胞进入静止状态会迫使 HIV 潜伏。
mBio. 2019 Mar 26;10(2):e00337-19. doi: 10.1128/mBio.00337-19.
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HIV "shock and kill" therapy: In need of revision.HIV“休克与清除”疗法:需要修订。
Antiviral Res. 2019 Jun;166:19-34. doi: 10.1016/j.antiviral.2019.03.008. Epub 2019 Mar 23.
6
Key Glycolytic Metabolites in Paralyzed Skeletal Muscle Are Altered Seven Days after Spinal Cord Injury in Mice.关键糖酵解代谢物在瘫痪的骨骼肌中发生改变,这是在小鼠脊髓损伤后 7 天发生的。
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7
PD-1 blockade potentiates HIV latency reversal ex vivo in CD4 T cells from ART-suppressed individuals.PD-1 阻断剂增强了 ART 抑制个体 CD4 T 细胞中 HIV 潜伏期的逆转。
Nat Commun. 2019 Feb 18;10(1):814. doi: 10.1038/s41467-019-08798-7.
8
Autophagy, EVs, and Infections: A Perfect Question for a Perfect Time.自噬、细胞外囊泡与感染:绝佳时机,绝佳问题。
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9
Programmed cell death-1 contributes to the establishment and maintenance of HIV-1 latency.程序性细胞死亡蛋白-1 有助于 HIV-1 潜伏的建立和维持。
AIDS. 2018 Jul 17;32(11):1491-1497. doi: 10.1097/QAD.0000000000001849.
10
CD32 is expressed on cells with transcriptionally active HIV but does not enrich for HIV DNA in resting T cells.CD32 表达于转录活跃的 HIV 细胞上,但不会使静止 T 细胞中的 HIV DNA 富集。
Sci Transl Med. 2018 Apr 18;10(437). doi: 10.1126/scitranslmed.aar6759.

利用 OMICs 方法发现候选 HIV-1 潜伏期生物标志物。

Discovery of candidate HIV-1 latency biomarkers using an OMICs approach.

机构信息

Department of Medical Microbiology and Immunology, Creighton University, Omaha, NE, USA.

Department of Medical Microbiology and Immunology, Creighton University, Omaha, NE, USA.

出版信息

Virology. 2021 Jun;558:86-95. doi: 10.1016/j.virol.2021.03.003. Epub 2021 Mar 11.

DOI:10.1016/j.virol.2021.03.003
PMID:33735754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10171037/
Abstract

Infection with HIV-1 remains uncurable due to reservoirs of latently infected cells. Any potential cure for HIV will require a mechanism to identify and target these cells in vivo. We created a panel of Jurkat cell lines latently infected with the HIV DuoFlo virus to identify candidate biomarkers of latency. SWATH mass spectrometry was used to compare the membrane proteomes of one of the cell lines to parental Jurkat cells. Several candidate proteins with significantly altered expression were identified. The differential expression of several candidates was validated in multiple latently infected cell lines. Three factors (LAG-3, CD147,CD231) were altered across numerous cell lines, but the expression of most candidate biomarkers was variable. These results confirm that phenotypic differences in latently infected cells exists and identify additional novel biomarkers. The variable expression of biomarkers across different cell clones suggests universal antigen-based detection of latently infected cells may require a multiplex approach.

摘要

由于潜伏感染细胞的存在,HIV-1 的感染仍然无法治愈。任何潜在的 HIV 治疗方法都需要一种机制来在体内识别和靶向这些细胞。我们创建了一组潜伏感染 HIV DuoFlo 病毒的 Jurkat 细胞系,以鉴定潜伏的候选生物标志物。SWATH 质谱法用于比较其中一个细胞系与亲本 Jurkat 细胞的膜蛋白质组。鉴定出几种表达明显改变的候选蛋白。在多个潜伏感染细胞系中验证了几个候选物的差异表达。三种因子(LAG-3、CD147、CD231)在多个细胞系中发生改变,但大多数候选生物标志物的表达是可变的。这些结果证实了潜伏感染细胞中存在表型差异,并确定了其他新的生物标志物。不同细胞克隆中生物标志物的可变表达表明,基于普遍抗原的潜伏感染细胞检测可能需要采用多重方法。