Evidence map›Paper›PMID 30195765›Full record

ArticleMolecular therapy. Nucleic acids2018

Inducing CCR5Δ32/Δ32 Homozygotes in the Human Jurkat CD4+ Cell Line and Primary CD4+ Cells by CRISPR-Cas9 Genome-Editing Technology.

Chunxia Qi, Dan Li, Xiangxiang Jiang, Xiaopeng Jia, Lingling Lu, Yanfeng Wang, Jinhuan Sun, Yiming Shao, Min Wei

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  5. Review
  6. HIV cure strategies: which ones are appropriate for Africa?Cellular and molecular life sciences : CMLS · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
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  16. Article
  17. Application of CRISPR/Cas9-Based Gene Editing in HIV-1/AIDS Therapy.Frontiers in cellular and infection microbiology · 2019
    Review
  18. Review
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

9 authors at 1 institution in 1 country.

Chunxia QiSchool of Medicine, Nankai University, Tianjin, China.
Dan LiNational Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Xiangxiang JiangSchool of Medicine, Nankai University, Tianjin, China.
Xiaopeng JiaSchool of Medicine, Nankai University, Tianjin, China.
Lingling LuSchool of Medicine, Nankai University, Tianjin, China.
Yanfeng WangSchool of Medicine, Nankai University, Tianjin, China.
Jinhuan SunSchool of Medicine, Nankai University, Tianjin, China.
Yiming ShaoSchool of Medicine, Nankai University, Tianjin, China; National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Min WeiSchool of Medicine, Nankai University, Tianjin, China; Nankai University Second People's Hospital, School of Medicine, Nankai University, Tianjin, China. Electronic address: weimin@nankai.edu.cn.
Nankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-C chemokine receptor type 5 (CCR5) is the main co-receptor for HIV entry into the target CD4+ cells, and homozygous CCR5Δ32/Δ32 cells are resistant to CCR5-tropic HIV infection. However, the CCR5Δ32/Δ32 homozygous donors in populations are rare. Here we developed a simple approach to induce CCR5Δ32/Δ32 homozygotes through CRISPR-Cas9 genome-editing technology. Designing a pair of single-guide RNA targeting the flank region of the CCR5Δ32 mutation locus, we applied the CRISPR-Cas9 and lentiviral packaging system to successfully convert wild-type CCR5 into CCR5Δ32/Δ32 homozygotes in the human Jurkat CD4+ cell line and primary CD4+ cells, exactly the same as the naturally occurring CCR5Δ32/Δ32 mutation. The successful rate is up to 20% in Jurkat cells but less in primary CD4+ cells. The modified CCR5Δ32/Δ32 CD4+ cells are resistant to CCR5-tropic HIV infection. Whole-genome sequencing revealed no apparent off-target sites. This approach has the promise to promote HIV/AIDS therapy from the only cured unique Berlin patient to a routine autologous cell-based therapy.

Indexed as

32AIDSCCR5ΔCD4+ cellsCRISPR-Cas9HIV

Identifiers

PMID30195765
PMCPMC6005807
OpenAlexW2808229735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.