Evidence map›Paper›PMID 38906865›Full record

ArticleNature communications2024

RPLP1 restricts HIV-1 transcription by disrupting C/EBPβ binding to the LTR.

Weijing Yang, Hong Wang, Zhaolong Li, Lihua Zhang, Jianhui Liu, Frank Kirchhoff, Chen Huan, Wenyan Zhang

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. The elite controller phenotype.Current opinion in HIV and AIDS · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The multifaceted roles of ribosomal P complex in cancer.World journal of surgical oncology · 2025
    Review
  9. Review
  10. Article
  11. 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

8 authors.

Weijing YangDepartment of Infectious Diseases, Infectious Diseases and Pathogen Biology Center, The First Hospital of Jilin University, Changchun, China.
Hong WangDepartment of Infectious Diseases, Infectious Diseases and Pathogen Biology Center, The First Hospital of Jilin University, Changchun, China.
Zhaolong LiDepartment of Infectious Diseases, Infectious Diseases and Pathogen Biology Center, The First Hospital of Jilin University, Changchun, China.
Lihua ZhangState Key Laboratory of Medical Proteomics, Dalian Institute of Chemical Physics, Chinese Academy of Science, Dalian, China.ORCID http://orcid.org/0000-0003-3798-2047
Jianhui LiuState Key Laboratory of Medical Proteomics, Dalian Institute of Chemical Physics, Chinese Academy of Science, Dalian, China.
Frank KirchhoffInstitute of Molecular Virology, Ulm University Medical Center, 89081, Ulm, Germany.ORCID http://orcid.org/0000-0002-7052-2360
Chen HuanDepartment of Infectious Diseases, Infectious Diseases and Pathogen Biology Center, The First Hospital of Jilin University, Changchun, China. lmsxsml@jlu.edu.cn.ORCID http://orcid.org/0009-0000-0930-2775
Wenyan ZhangDepartment of Infectious Diseases, Infectious Diseases and Pathogen Biology Center, The First Hospital of Jilin University, Changchun, China. zhangwenyan@jlu.edu.cn.ORCID http://orcid.org/0000-0003-4507-521X

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) CRC 1279National Natural Science Foundation of China (National Science Foundation of China) 81930062
6 · The paper itself

Abstract

Long-term non-progressors (LTNPs) of HIV-1 infection may provide important insights into mechanisms involved in viral control and pathogenesis. Here, our results suggest that the ribosomal protein lateral stalk subunit P1 (RPLP1) is expressed at higher levels in LTNPs compared to regular progressors (RPs). Functionally, RPLP1 inhibits transcription of clade B HIV-1 strains by occupying the C/EBPβ binding sites in the viral long terminal repeat (LTR). This interaction requires the α-helixes 2 and 4 domains of RPLP1 and is evaded by HIV-1 group M subtype C and group N, O and P strains that do not require C/EBPβ for transcription. We further demonstrate that HIV-1-induced translocation of RPLP1 from the cytoplasm to the nucleus is essential for antiviral activity. Finally, knock-down of RPLP1 promotes reactivation of latent HIV-1 proviruses. Thus, RPLP1 may play a role in the maintenance of HIV-1 latency and resistance to RPLP1 restriction may contribute to the effective spread of clade C HIV-1 strains.

Indexed as

CCAAT-Enhancer-Binding Protein-betaHIV-1HIV InfectionsHIV Long Terminal RepeatRibosomal ProteinsBinding SitesCell NucleusGene Expression Regulation, ViralHEK293 CellsHumansPhosphoproteinsProtein BindingTranscription, GeneticVirus LatencyCCAAT-Enhancer-Binding Protein-betaPhosphoproteinsribosomal phosphoprotein P1Ribosomal Proteins

Identifiers

PMID38906865
PMCPMC11192919

What OpenQuestion holds

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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.