Evidence map›Paper›PMID 24568220›Full record

ArticleHuman gene therapy methods2014

Dual adeno-associated virus vectors result in efficient in vitro and in vivo expression of an oversized gene, MYO7A.

Frank M Dyka, Sanford L Boye, Vince A Chiodo, William W Hauswirth, Shannon E Boye

Abstract read
In one paragraph

Article in Human gene therapy methods, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 126 citations in OpenAlex.

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  15. Dual-AAV vector-mediated expression ofMolecular therapy. Methods & clinical development · 2023
    Article
  16. Successful large gene augmentation of USH2A with non-viral episomal vectors.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  17. Article
  18. Developing New Vectors for Retinal Gene Therapy.Cold Spring Harbor perspectives in medicine · 2023
    Article
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21 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Frank M DykaDepartment of Ophthalmology, College of Medicine, University of Florida , Gainesville, FL 32610.
Sanford L Boye
Vince A Chiodo
William W Hauswirth
Shannon E Boye
University of Florida · US

Funding

Vision Research CoreP30EY021721 · NEI · UNIVERSITY OF FLORIDA · PI HAUSWIRTH, WILLIAM W · 2011 to 2015
$2.8M
NEI NIH HHS P30 EY021721NEI NIH HHS P30EY021721
6 · The paper itself

Abstract

Usher syndrome 1B (USH1B) is a severe, autosomal recessive, deaf-blind disorder caused by mutations in myosin 7A (MYO7A). Patients are born profoundly deaf and exhibit progressive loss of vision starting in their first decade. MYO7A is expressed in human photoreceptors and retinal pigment epithelium, but disease pathology begins in photoreceptors, highlighting the need to develop a gene replacement strategy that effectively targets this cell type. For its safety and efficacy in clinical trials and ability to transduce postmitotic photoreceptors, we have focused on developing a clinically applicable adeno-associated virus (AAV) platform for delivering full-length MYO7A cDNA (∼6.7 kb). Packaging of full-length MYO7A cDNA in AAV produces vectors with heterogeneous, fragmented genomes ("fAAV") capable of reconstituting full-length cDNA postinfection. We previously showed that fAAV vectors effectively delivered full-length MYO7A in vitro and in vivo. However, fAAV vectors are relatively inefficient and their heterogeneous genomes preclude definitive characterization, a drawback for clinical translatability. The aim of this study was to overcome these limitations by creating dual-AAV-vector platforms for USH1B with defined genomes. Human MYO7A was cloned in AAV vector pairs, each containing genomes <5 kb and intact inverted terminal repeats. One vector contained a promoter and 5' portion of the cDNA and the partner vector contained a 3' portion and polyadenylation signal. "Simple overlap" vectors share a central part of the MYO7A cDNA sequence. "Trans-splicing" and "hybrid" vectors utilize splice donor and acceptor sites with and without an additional central recombinogenic sequence, respectively. Vector pairs expressed full-length MYO7A in vitro and in vivo with equal or higher efficiency than fAAV, with a hybrid platform being most efficient. Importantly, analysis of MYO7A mRNA derived from each dual-vector platform revealed 100% fidelity to the predicted sequence. Our results suggest that dual AAV vectors with defined genetic payloads are a potential treatment option for USH1B.

Indexed as

Gene Expression RegulationAnimalsCloning, MolecularDependovirusElectrophoresis, Polyacrylamide GelGenetic VectorsHEK293 CellsHumansImmunohistochemistryMiceMice, Inbred C57BLMyosinsMyosin VIIaRecombinant ProteinsRetinaRNA SplicingMYO7A protein, humanMyo7a protein, mouseMyosinsMyosin VIIaRecombinant Proteins

Identifiers

PMID24568220
PMCPMC3991978
OpenAlexW2317202809

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.