Evidence map›Paper›PMID 33053801›Full record

ArticleViruses2020

Targeted Chromatinization and Repression of HIV-1 Provirus Transcription with Repurposed CRISPR/Cas9.

Alex Olson, Binita Basukala, Seunghee Lee, Matthew Gagne, Wilson W Wong, Andrew J Henderson

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2020. 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
1.5field-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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. CRISPR/Cas9 for achieving postintervention HIV control.Current opinion in HIV and AIDS · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. CRISPR/Cas9: a tool to eradicate HIV-1.AIDS research and therapy · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
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  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

6 authors at 1 institution in 1 country.

Alex OlsonDepartment of Medicine and Microbiology, Boston University School of Medicine, Boston, MA 02118, USA.
Binita BasukalaDepartment of Biology, Boston University, Boston, MA 02215, USA.
Seunghee LeeBiomedical Engineering and Biological Design Center, Boston University, Boston, MA 02215, USA.
Matthew GagneDepartment of Medicine and Microbiology, Boston University School of Medicine, Boston, MA 02118, USA.
Wilson W WongBiomedical Engineering and Biological Design Center, Boston University, Boston, MA 02215, USA.
Andrew J HendersonDepartment of Medicine and Microbiology, Boston University School of Medicine, Boston, MA 02118, USA.
Boston University · US

Funding

Translational ScienceP30AI042853 · NIAID · MIRIAM HOSPITAL · PI CURT G BECKWITH, DEBBIE M. CHENG · 1998 to 2026
$51.7M
Single nuclei transcriptomics of Alzheimer's brain diseaseR61DA047032 · NIDA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI CHENG, CHRISTINE, HENDERSON, ANDREW J · 2018 to 2020
$3.5M
Signals that establish and maintain HIV latencyR01AI138960 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2018 to 2022
$2.2M
Effect of opioid use disorder on HIV latent reservoirs and immune dysfunction assessed by single-cell transcriptomicsR33DA047032 · NIDA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI CHENG, CHRISTINE, HENDERSON, ANDREW J · 2021 to 2022
$1.8M
NIAID NIH HHS P30 AI042853NIAID NIH HHS R01 AI138960NIDA NIH HHS R33 DA047032NIDA NIH HHS R61 DA047032NIH HHS R01 AI138960
6 · The paper itself

Abstract

The major barrier to HIV-1 cure is the persistence of latent provirus, which is not eradicated by antiretroviral therapy. The "shock and kill" approach entails stimulating viral production with latency-reversing agents followed by the killing of cells actively producing the virus by immune clearance. However, this approach does not induce all intact proviruses, leaving a residual reservoir. CRISPR/Cas9 has been utilized to excise integrated Human Immunodeficiency Virus (HIV) DNA from infected cells in an RNA-guided, sequence-specific manner. Here, we seek to epigenetically silence the proviral DNA by introducing nuclease-deficient disabled Cas9 (dCas9) coupled with a transcriptional repressor domain derived from Kruppel-associated box (KRAB). We show that specific guide RNAs (gRNAs) and dCas9-KRAB repress HIV-1 transcription and reactivation of latent HIV-1 provirus. This repression is correlated with chromatin changes, including decreased H3 histone acetylation and increased histone H3 lysine 9 trimethylation, histone marks that are associated with transcriptional repression. dCas9-KRAB-mediated inhibition of HIV-1 transcription suggests that CRISPR can be engineered as a tool for block-and-lock strategies.

Indexed as

AcetylationCell LineClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsEpigenesis, GeneticHEK293 CellsHistonesHIV-1HIV InfectionsHIV Long Terminal RepeatHumansJurkat CellsMethylationProvirusesRepressor ProteinsRNA, Guide, CRISPR-Cas SystemsHistonesRepressor ProteinsRNA, Guide, CRISPR-Cas SystemsZNF350 protein, humanchromatinCRISPRHIV latencyHIV transcription

Identifiers

PMID33053801
PMCPMC7600714
OpenAlexW3091973224

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.