Evidence map›Paper›PMID 30401776›Full record

ArticlemBio2018

Splicing Factor 3B Subunit 1 Interacts with HIV Tat and Plays a Role in Viral Transcription and Reactivation from Latency.

George B Kyei, Shanshan Meng, Rashmi Ramani, Austin Niu, Chandraiah Lagisetti, Thomas R Webb, Lee Ratner

Open access · goldAbstract read
In one paragraph

Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. SuppressedInternational journal of molecular sciences · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. HIV cure strategies: which ones are appropriate for Africa?Cellular and molecular life sciences : CMLS · 2022
    Review
  10. Article
  11. HibeRNAtion: HIV-1 RNA Metabolism and Viral Latency.Frontiers in cellular and infection microbiology · 2022
    Review
  12. Article
  13. Cure and Long-Term Remission Strategies.Methods in molecular biology (Clifton, N.J.) · 2022
    Review
  14. Article
  15. Article
  16. 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

7 authors at 3 institutions in 2 countries.

George B KyeiDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA g.kyei@wustl.edu.
Shanshan MengDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Rashmi RamaniDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Austin NiuDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Chandraiah LagisettiDivision of Biosciences, SRI International, Menlo Park, California, USA.
Thomas R WebbDivision of Biosciences, SRI International, Menlo Park, California, USA.
Lee RatnerDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Washington University in St. Louis · USSRI International · USUniversity of Ghana · GH

Funding

CONTROL OF HIV REPLICATION BY CYCLIN L2K08AI120854 · NIAID · WASHINGTON UNIVERSITY · PI KYEI, GEORGE · 2015 to 2019
$807k
NIAID NIH HHS K08 AI120854
6 · The paper itself

Abstract

The main obstacle to an HIV cure is the transcriptionally inert proviruses that persist in resting CD4 T cells and other reservoirs. None of the current approaches has significantly reduced the size of the viral reservoir. Hence, alternative approaches, such as permanent blocking of viral transcription, to achieve a sustained remission, need urgent attention. To identify cellular factors that may be important for this approach, we sought for host targets that when altered could block HIV transcription and reactivation. Here, we identified splicing factor 3B subunit 1 (SF3B1) as a critical HIV dependency factor required for viral replication. SF3B1 is a splicing factor involved in directing chromatin and nascent gene transcripts to appropriate splice sites. Inhibitors of SF3B1 are currently in development for cancer and have been found to be nontoxic to normal cells compared to malignant cells. Knockdown of SF3B1 abrogated HIV replication in all cell types tested. SF3B1 interacted with viral protein Tat

Indexed as

Virus ActivationVirus LatencyChromatinCyclohexylaminesHEK293 CellsHIV-1HumansJurkat CellsMacrophagesPhosphoproteinsRNA, Small InterferingRNA Splicing FactorsSpiro Compoundstat Gene Products, Human Immunodeficiency VirusTHP-1 CellsTranscription, Genetic5-((4-(5-(7,7-dimethyl-1,6-dioxaspiro(2.5)octan-5-yl)-3-methylpenta-2,4-dien-1-yl)cyclohexyl)amino)-5-oxopent-3-en-2-yl methylcarbamateChromatinCyclohexylaminesPhosphoproteinsRNA, Small InterferingRNA Splicing FactorsSF3B1 protein, humanSpiro Compoundstat Gene Products, Human Immunodeficiency Virusblock and lockHIV cureHIV transcriptionhuman immunodeficiency viruslatencyreactivation

Identifiers

PMID30401776
PMCPMC6222122
OpenAlexW2899837367

What OpenQuestion holds

Textmetadata
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.