Evidence map›Paper›PMID 24945407›Full record

ArticlePLoS computational biology2014

A quantitative comparison of anti-HIV gene therapy delivered to hematopoietic stem cells versus CD4+ T cells.

Borislav Savkovic, James Nichols, Donald Birkett, Tanya Applegate, Scott Ledger, Geoff Symonds, John M Murray

Abstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS.Frontiers in cellular and infection microbiology · 2020
    Review
  3. Article
  4. Review
  5. HIV Impacts CD34Frontiers in immunology · 2019
    Article
  6. Article
  7. Article
  8. Review
  9. 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

7 authors.

Borislav SavkovicSchool of Mathematics and Statistics, University of New South Wales, Sydney, Australia.
James NicholsSchool of Mathematics and Statistics, University of New South Wales, Sydney, Australia.
Donald BirkettDepartment of Clinical Pharmacology, Flinders University, Adelaide, Australia.
Tanya ApplegateKirby Institute, University of New South Wales, Sydney, Australia.
Scott LedgerFaculty of Medicine, University of New South Wales, Sydney, Australia.
Geoff SymondsSt Vincent's Centre for Applied Medical Research, Darlinghurst, New South Wales, Sydney, Australia; Calimmune Pty Ltd, Darlinghurst, New South Wales, Australia.
John M MurraySchool of Mathematics and Statistics, University of New South Wales, Sydney, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene therapy represents an alternative and promising anti-HIV modality to highly active antiretroviral therapy. It involves the introduction of a protective gene into a cell, thereby conferring protection against HIV. While clinical trials to date have delivered gene therapy to CD4+T cells or to CD34+ hematopoietic stem cells (HSC), the relative benefits of each of these two cellular targets have not been conclusively determined. In the present analysis, we investigated the relative merits of delivering a dual construct (CCR5 entry inhibitor + C46 fusion inhibitor) to either CD4+T cells or to CD34+ HSC. Using mathematical modelling, we determined the impact of each scenario in terms of total CD4+T cell counts over a 10 year period, and also in terms of inhibition of CCR5 and CXCR4 tropic virus. Our modelling determined that therapy delivery to CD34+ HSC generally resulted in better outcomes than delivery to CD4+T cells. An early one-off therapy delivery to CD34+ HSC, assuming that 20% of CD34+ HSC in the bone marrow were gene-modified (G+), resulted in total CD4+T cell counts ≥ 180 cells/ µL in peripheral blood after 10 years. If the uninfected G+ CD4+T cells (in addition to exhibiting lower likelihood of becoming productively infected) also exhibited reduced levels of bystander apoptosis (92.5% reduction) over non gene-modified (G-) CD4+T cells, then total CD4+T cell counts of ≥ 350 cells/ µL were observed after 10 years, even if initially only 10% of CD34+ HSC in the bone marrow received the protective gene. Taken together our results indicate that: 1.) therapy delivery to CD34+ HSC will result in better outcomes than delivery to CD4+T cells, and 2.) a greater impact of gene therapy will be observed if G+ CD4+T cells exhibit reduced levels of bystander apoptosis over G- CD4+T cells.

Indexed as

Computer SimulationGenetic TherapyHIV InfectionsModels, BiologicalAntigens, CD34CD4-Positive T-LymphocytesComputational BiologyDisease ProgressionGene Transfer TechniquesHematopoietic Stem CellsHIV-1HIV Fusion InhibitorsHumansReceptors, CCR5Recombinant Fusion ProteinsAntigens, CD34C46 HIV-1 fusion inhibitory peptideCCR5 protein, humanHIV Fusion InhibitorsReceptors, CCR5Recombinant Fusion Proteins

Identifiers

PMID24945407
PMCPMC4063676

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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.