Evidence map›Paper›PMID 32581100›Full record

ArticleJournal of virology2020

NF-κB-Interacting Long Noncoding RNA Regulates HIV-1 Replication and Latency by Repressing NF-κB Signaling.

Hong Wang, Yue Liu, Chen Huan, Jing Yang, Zhaolong Li, Baisong Zheng, Yingchao Wang, Wenyan Zhang

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses.International journal of molecular sciences · 2024
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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

8 authors at 2 institutions in 1 country.

Hong Wang *Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Yue Liu *Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Chen HuanInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Jing YangInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Zhaolong LiInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Baisong ZhengInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China.
Yingchao WangDepartment of Hepatobiliary Pancreatic Surgery, The First Hospital of Jilin University, Changchun, People's Republic of China.
Wenyan ZhangInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, People's Republic of China zhangwenyan@jlu.edu.cn.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NF-κB-interacting long noncoding RNA (NKILA) was recently identified as a negative regulator of NF-κB signaling and plays an important role in the development of various cancers. It is well known that NF-κB-mediated activation of human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR)-driven gene expression is required for HIV-1 transcription and reactivation of latency. However, whether NKILA plays essential roles in HIV-1 replication and latency is unclear. Here, by ectopic expression and silencing experiments, we demonstrate that NKILA potently inhibits HIV-1 replication in an NF-κB-dependent manner by suppressing HIV-1 LTR promoter activity. Moreover, NKILA showed broad-spectrum inhibition on the replication of HIV-1 clones with different coreceptor tropisms as well as on LTR activity of various HIV-1 clinical subtypes. Chromatin immunoprecipitation (ChIP) assays revealed that NKILA expression abolishes the recruitment of p65 to the duplicated κB binding sites in the HIV-1 LTR. NKILA mutants disrupting NF-κB inhibition also lost the ability to inhibit HIV-1 replication. Notably, HIV-1 infection or reactivation significantly downregulated NKILA expression in T cells in order to facilitate viral replication. Downregulated NKILA was mainly due to reduced acetylation of histone K27 on the promoter of NKILA by HIV-1 infection, which blocks NKILA expression. Knockdown of NKILA promoted the reactivation of latent HIV-1 upon phorbol myristate acetate (PMA) stimulation, while ectopic NKILA suppressed the reactivation in a well-established clinical model of withdrawal of azidothymidine (AZT)

Indexed as

Anti-HIV AgentsCD4-Positive T-LymphocytesChromatin ImmunoprecipitationGene Expression Regulation, ViralHEK293 CellsHIV-1HIV InfectionsHIV Long Terminal RepeatHumansNF-kappa BPhosphorylationRNA, Long NoncodingSignal TransductionVirus LatencyVirus ReplicationAnti-HIV Agentslong noncoding RNA NKILA, humanNF-kappa BRNA, Long Noncodingantiviral activityHIV-1 latencyHIV-1 replicationlncRNANF-κBNKILA

Identifiers

PMID32581100
PMCPMC7431781
OpenAlexW3036730159

What OpenQuestion holds

Textmetadata
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.