Evidence map›Paper›PMID 30670656›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat.

Manabu Taura, Eric Song, Ya-Chi Ho, Akiko Iwasaki

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Complex Relationships between HIV-1 Integrase and Its Cellular Partners.International journal of molecular sciences · 2022
    Review
  18. APOBEC3A regulates transcription from interferon-stimulated response elements.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Manabu TauraDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Eric SongDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Ya-Chi HoDepartment of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520.
Akiko IwasakiDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; akiko.iwasaki@yale.edu.ORCID 0000-0002-7824-9856
Yale University · USHoward Hughes Medical Institute · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Howard Hughes Medical InstituteNIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

HIV-1 integrates into the genome of target cells and establishes latency indefinitely. Understanding the molecular mechanism of HIV-1 latency maintenance is needed for therapeutic strategies to combat existing infection. In this study, we found an unexpected role for Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A, abbreviated "A3A") in maintaining the latency state within HIV-1-infected cells. Overexpression of A3A in latently infected cell lines led to lower reactivation, while knockdown or knockout of A3A led to increased spontaneous and inducible HIV-1 reactivation. A3A maintains HIV-1 latency by associating with proviral DNA at the 5' long terminal repeat region, recruiting KAP1 and HP1, and imposing repressive histone marks. We show that knockdown of A3A in latently infected human primary CD4 T cells enhanced HIV-1 reactivation. Collectively, we provide evidence and a mechanism by which A3A reinforces HIV-1 latency in infected CD4 T cells.

Indexed as

Epigenesis, GeneticGene SilencingHIV Long Terminal RepeatVirus LatencyCD4-Positive T-LymphocytesCell LineCytidine DeaminaseGene Expression Regulation, ViralHIV-1HIV InfectionsHumansNF-kappa BProtein BindingProtein Interaction Domains and MotifsProteinsSequence DeletionAPOBEC3A protein, humanCytidine DeaminaseNF-kappa BProteinsSp1 Transcription Factorepigenetic regulationreactivationT cellsTRIM28viral latency

Identifiers

PMID30670656
PMCPMC6369738
OpenAlexW2911795872

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.