Evidence map›Paper›PMID 23364313›Full record

ReviewGene therapy2013

Combinatorial anti-HIV gene therapy: using a multipronged approach to reach beyond HAART.

C W Peterson, P Younan, K R Jerome, H-P Kiem

Open access · bronzeAbstract readReview
In one paragraph

Review in Gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Drug delivery strategies and systems for HIV/AIDS pre-exposure prophylaxis and treatment.Journal of controlled release : official journal of the Controlled Release Society · 2015
    Review
  14. Review
  15. Article
  16. A new hypothesis on HIV cure.F1000Research · 2015
    Article
  17. Genetically modified hematopoietic stem cell transplantation for HIV-1-infected patients: can we achieve a cure?Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Review
  18. 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 3 institutions in 2 countries.

C W PetersonClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
P Younan
K R Jerome
H-P Kiem
Fred Hutch Cancer Center · USSeattle University · USUniversity of Washington · US

Funding

ZFN-Modified Stem Cells for HIV EradicationU19AI096111 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GREGORY, PHILIP D · 2011 to 2015
$20.8M
Cord Blood Expansion/Transplantation Nonhuman PrimateR01HL084345 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KIEM, HANS-PETER · 2006 to 2009
$2.8M
Development of Novel AIDS Gene Therapy Strategies in the Macaque SHIV ModelR01AI080326 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KIEM, HANS-PETER · 2009 to 2012
$2.2M
NHLBI NIH HHS R01 HL084345NHLBI NIH HHS R01 HL84345NIAID NIH HHS R01 AI080326NIAID NIH HHS R01 AI80326NIAID NIH HHS U19 AI 096111NIAID NIH HHS U19 AI096111
6 · The paper itself

Abstract

The 'Berlin Patient', who maintains suppressed levels of HIV viremia in the absence of antiretroviral therapy, continues to be a standard bearer in HIV eradication research. However, the unique circumstances surrounding his functional cure are not applicable to most HIV(+) patients. To achieve a functional or sterilizing cure in a greater number of infected individuals worldwide, combinatorial treatments, targeting multiple stages of the viral life cycle, will be essential. Several anti-HIV gene therapy approaches have been explored recently, including disruption of the C-C chemokine receptor 5 (CCR5) and CXC chemokine receptor 4 (CXCR4) coreceptor loci in CD4(+) T cells and CD34(+) hematopoietic stem cells. However, less is known about the efficacy of these strategies in patients and more relevant HIV model systems such as non-human primates (NHPs). Combinatorial approaches, including genetic disruption of integrated provirus, functional enhancement of endogenous restriction factors and/or the use of pharmacological adjuvants, could amplify the anti-HIV effects of CCR5/CXCR4 gene disruption. Importantly, delivering gene disruption molecules to genetic sites of interest will likely require optimization on a cell type-by-cell type basis. In this review, we highlight the most promising gene therapy approaches to combat HIV infection, methods to deliver these therapies to hematopoietic cells and emphasize the need to target viral replication pre- and post-entry to mount a suitably robust defense against spreading infection.

Indexed as

Antiretroviral Therapy, Highly ActiveAntigens, CD34CD4-Positive T-LymphocytesGenetic TherapyHematopoietic Stem CellsHIV-1HIV InfectionsHumansMolecular Targeted TherapyReceptors, CCR5Receptors, CXCR4Virus ReplicationAntigens, CD34CXCR4 protein, humanReceptors, CCR5Receptors, CXCR4

Identifiers

PMID23364313
PMCPMC3725618
OpenAlexW2091806378

What OpenQuestion holds

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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.