Evidence map›Paper›PMID 27795436›Full record

ArticleJournal of virology2017

Naf1 Regulates HIV-1 Latency by Suppressing Viral Promoter-Driven Gene Expression in Primary CD4+ T Cells.

Chuan Li, Hai-Bo Wang, Wen-Dong Kuang, Xiao-Xin Ren, Shu-Ting Song, Huan-Zhang Zhu, Qiang Li, Li-Ran Xu, Hui-Jun Guo, Li Wu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

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  12. Barriers for HIV Cure: The Latent Reservoir.AIDS research and human retroviruses · 2018
    Review
  13. Article
  14. Review
  15. Scaffold attachment factor B suppresses HIV-1 infection of CD4The Journal of biological chemistry · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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

11 authors at 7 institutions in 2 countries.

Chuan LiCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Hai-Bo WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Wen-Dong KuangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Xiao-Xin RenCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Shu-Ting SongCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Huan-Zhang ZhuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China.
Qiang LiKey Laboratory of Prevention and Treatment with Traditional Chinese Medicine of Viral Infectious 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 of Viral Infectious 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 of Viral Infectious Disease, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Li WuCenter for Retrovirus Research, Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA wu.840@osu.edu jh_wang@sibs.ac.cn.
Jian-Hua WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China wu.840@osu.edu jh_wang@sibs.ac.cn.
Chinese Academy of Sciences · CNFirst Affiliated Hospital of Henan University of Traditional Chinese Medicine · CNInstitut Pasteur of Shanghai · CNGuangzhou Medical University · CNHenan University of Traditional Chinese Medicine · CNState Key Laboratory of Genetic EngineeringThe Ohio State University · US

Funding

Mechanisms of SAMHD1-mediated HIV-1 restriction in dendritic cellsR01AI104483 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2013 to 2016
$1.5M
HIV-1 Nef Interaction with Nef-associated Factor 1 Regulates Viral LatencyR01AI120209 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2015 to 2017
$600k
Mechanisms of HIV-1 RNA Methylation in Regulating Viral ReplicationR56AI127667 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2016 to 2016
$400k
Novel role of SAMHD1 as a tumor suppressor in cutaneous T-cell lymphomasR21CA181997 · NCI · OHIO STATE UNIVERSITY · PI WU, LI · 2014 to 2015
$368k
NCI NIH HHS R21 CA181997NIAID NIH HHS R01 AI104483NIAID NIH HHS R01 AI120209NIAID NIH HHS R56 AI127667
6 · The paper itself

Abstract

HIV-1 latency is characterized by reversible silencing of viral transcription driven by the long terminal repeat (LTR) promoter of HIV-1. Cellular and viral factors regulating LTR activity contribute to HIV-1 latency, and certain repressive cellular factors modulate viral transcription silencing. Nef-associated factor 1 (Naf1) is a host nucleocytoplasmic shuttling protein that regulates multiple cellular signaling pathways and HIV-1 production. We recently reported that nuclear Naf1 promoted nuclear export of unspliced HIV-1 gag mRNA, leading to increased Gag production. Here we demonstrate new functions of Naf1 in regulating HIV-1 persistence. We found that Naf1 contributes to the maintenance of HIV-1 latency by inhibiting LTR-driven HIV-1 gene transcription in a nuclear factor kappa B-dependent manner. Interestingly, Naf1 knockdown significantly enhanced viral reactivation in both latently HIV-1-infected Jurkat T cells and primary central memory CD4 IMPORTANCE: HIV-1 latency is characterized mainly by a reversible silencing of LTR promoter-driven transcription of an integrated provirus. Cellular and viral proteins regulating LTR activity contribute to the modulation of HIV-1 latency. In this study, we found that the host protein Naf1 inhibited HIV-1 LTR-driven transcription of HIV genes and contributed to the maintenance of HIV-1 latency. Our findings provide new insights into the effects of host modulation on HIV-1 latency, which may lead to a potential therapeutic strategy for HIV persistence by targeting the Naf1 protein.

Indexed as

Gene Expression Regulation, ViralCD4-Positive T-LymphocytesCell Nucleusgag Gene Products, Human Immunodeficiency VirusGene SilencingHIV-1HIV InfectionsHIV Long Terminal RepeatHost-Pathogen InteractionsHumansJurkat CellsNF-kappa BPrimary Cell CulturePromoter Regions, GeneticRibonucleoproteinsRNA, Messengergag Gene Products, Human Immunodeficiency VirusNAF1 protein, humanNF-kappa BRibonucleoproteinsRNA, MessengerRNA, Small InterferingRNA, ViralHIV-1 latencyHIV-1 Nef-associated factor 1NF-κBtranscription

Identifiers

PMID27795436
PMCPMC5165213
OpenAlexW2533244977

What OpenQuestion holds

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Registered trials

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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.