Evidence map›Paper›PMID 38741006›Full record

ArticleScientific reports2024

CRISPR/Cas9 genome editing of CCR5 combined with C46 HIV-1 fusion inhibitor for cellular resistant to R5 and X4 tropic HIV-1.

Wannisa Khamaikawin, Chonticha Saisawang, Boonrat Tassaneetrithep, Kanit Bhukhai, Phetcharat Phanthong, Suparerk Borwornpinyo, Angsana Phuphuakrat, Ekawat Pasomsub, Sujittra Chaisavaneeyakorn, Usanarat Anurathapan and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 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. Review
  2. Review
  3. Review
  4. Review
  5. Searching for a HIV-1 Cure.Theranostics · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. CRISPR/Cas9 for achieving postintervention HIV control.Current opinion in HIV and AIDS · 2025
    Review
  10. Review
  11. 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

12 authors.

Wannisa KhamaikawinFaculty of Medicine, King Mongkut's Institute of Technology Ladkrabang, Bangkok, 10520, Thailand.
Chonticha SaisawangCenter for Advanced Therapeutics, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhon Pathom, 73170, Thailand.
Boonrat TassaneetrithepCenter of Research Excellence in Immunoregulation, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand.
Kanit BhukhaiDepartment of Physiology, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Phetcharat PhanthongDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Suparerk BorwornpinyoDepartment of Biotechnology, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Angsana PhuphuakratDepartment of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Ekawat PasomsubDepartment of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Sujittra ChaisavaneeyakornDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Usanarat AnurathapanDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Nopporn ApiwattanakulDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Suradej HongengDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand. suradej.hon@mahidol.ac.th.

Funding

King Mongkut's Institute of Technology Ladkrabang 2563-0216006Office of National Higher Education Science Research and Innovation Policy Council through the Program Management Unit for Human Resources & Institutional Development, Research and Innovation (PMU-B) B05F630063
6 · The paper itself

Abstract

Hematopoietic stem-cell (HSC) transplantation using a donor with a homozygous mutation in the HIV co-receptor CCR5 (CCR5Δ32/Δ32) holds great promise as a cure for HIV-1. Previously, there were three patients that had been reported to be completely cured from HIV infection by this approach. However, finding a naturally suitable Human Leukocyte Antigen (HLA)-matched homozygous CCR5Δ32 donor is very difficult. The prevalence of this allele is only 1% in the Caucasian population. Therefore, additional sources of CCR5Δ32/Δ32 HSCs are required. The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated (Cas) system is one method to mediate CCR5 knockout in HSCs that has been successfully employed as a gene editing tool in clinical trials. Additional anti-HIV-1 strategies are still required for broad-spectrum inhibition of HIV-1 replication. Here in this study, we combined an additional anti-HIV-1 therapy, which is C46, a cell membrane-anchored HIV-1 fusion inhibitor with the CRISPR/Cas9 mediated knockout CCR5. The combined HIV-1 therapeutic genes were investigated for the potential prevention of both CCR5 (R5)- and CXCR4 (X4)-tropic HIV-1 infections in the MT4CCR5 cell line. The combinatorial CRISPR/Cas9 therapies were superior compared to single method therapy for achieving the HIV-1 cure strategy and shows potential for future applications.

Indexed as

CRISPR-Cas SystemsGene EditingHIV-1HIV Fusion InhibitorsHIV InfectionsReceptors, CCR5Cell LineHumansRecombinant Fusion ProteinsVirus ReplicationC46 HIV-1 fusion inhibitory peptideCCR5 protein, humanHIV Fusion InhibitorsReceptors, CCR5Recombinant Fusion ProteinsC46 HIV-1 fusion inhibitorCCR5 CRISPR/Cas9HIV-1 gene therapy

Identifiers

PMID38741006
PMCPMC11091187

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Registered trials

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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.