Evidence map›Paper›PMID 27698388›Full record

ArticleScientific reports2016

The variances of Sp1 and NF-κB elements correlate with the greater capacity of Chinese HIV-1 B'-LTR for driving gene expression.

Di Qu, Chuan Li, Feng Sang, Qiang Li, Zhi-Qiang Jiang, Li-Ran Xu, Hui-Jun Guo, Chiyu Zhang, Jian-Hua Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Di QuCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Chuan LiCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Feng SangKey laboratory of Prevention and Treatment with Traditional Chinese Medicine on Viral Infection Disease, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Qiang LiKey laboratory of Prevention and Treatment with Traditional Chinese Medicine on Viral Infection Disease, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Zhi-Qiang JiangKey laboratory of Prevention and Treatment with Traditional Chinese Medicine on Viral Infection Disease, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Li-Ran XuKey laboratory of Prevention and Treatment with Traditional Chinese Medicine on Viral Infection Disease, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Hui-Jun GuoKey laboratory of Prevention and Treatment with Traditional Chinese Medicine on Viral Infection Disease, the First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Chiyu ZhangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Jian-Hua WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Henan University of Traditional Chinese Medicine · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 5' end of HIV-1 long terminal repeat (LTR) serves as a promoter that plays an essential role in driving viral gene transcription. Manipulation of HIV-1 LTR provides a potential therapeutic strategy for suppressing viral gene expression or excising integrated provirus. Subtype-specific genetic diversity in the LTR region has been observed. The minor variance of LTR, particularly in the transcription factor binding sites, can have a profound impact on its activity. However, the LTR profiles from major endemic Chinese subtypes are not well characterized. Here, by characterizing the sequences and functions of LTRs from endemic Chinese HIV-1 subtypes, we showed that nucleotide variances of Sp1 core promoter and NF-κB element are associated with varied LTR capacity for driving viral gene transcription. The greater responsiveness of Chinese HIV-1 B'-LTR for driving viral gene transcription upon stimulation is associated with an increased level of viral reactivation. Moreover, we demonstrated that the introduction of CRISPR/dead Cas9 targeting Sp1 or NF-κB element suppressed viral gene expression. Taken together, our study characterized LTRs from endemic HIV-1 subtypes in China and suggests a potential target for the suppression of viral gene expression and a novel strategy that facilitates the accomplishment of a functional cure.

Indexed as

HIV-1HIV Long Terminal RepeatResponse ElementsChinaFemaleGene Expression Regulation, ViralHEK293 CellsHumansMaleNF-kappa BSp1 Transcription FactorNF-kappa BSP1 protein, humanSp1 Transcription Factor

Identifiers

PMID27698388
PMCPMC5048295
OpenAlexW2528643102

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.