ArticleHuman gene therapy methods2015
AAV-8 is more efficient than AAV-9 in transducing neonatal dog heart.
Article in Human gene therapy methods, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Systemic delivery of AAV5, AAV8, and AAV9 packaging a C5-12-microdystrophin-FLAG expression cassette in non-human primates.Molecular therapy. Methods & clinical development · 2025Article
- Adeno-Associated Virus 8 and 9 Myofibre Type/Size Tropism Profiling Reveals Therapeutic Effect of Microdystrophin in Canines.Journal of cachexia, sarcopenia and muscle · 2025Article
- Evaluation of an AAV9-mini-dystrophin gene therapy candidate in a rat model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2023Article
- Improved transduction of canine X-linked muscular dystrophy with rAAV9-microdystrophin via multipotent MSC pretreatment.Molecular therapy. Methods & clinical development · 2021Article
- New and Developing Therapies in Spinal Muscular Atrophy: From Genotype to Phenotype to Treatment and Where Do We Stand?International journal of molecular sciences · 2020Review
- Transduction Efficiency of Adeno-Associated Virus Serotypes After Local Injection in Mouse and Human Skeletal Muscle.Human gene therapy · 2020Article
- Systemic Delivery of Adeno-Associated Viral Vectors in Mice and Dogs.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Micro-Dystrophin Gene Therapy Goes Systemic in Duchenne Muscular Dystrophy Patients.Human gene therapy · 2018Article
- Myoediting: Toward Prevention of Muscular Dystrophy by Therapeutic Genome Editing.Physiological reviews · 2018Review
- Nanotherapy for Duchenne muscular dystrophy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
- Use of Adeno-Associated Virus Vector for Cardiac Gene Delivery in Large-Animal Surgical Models of Heart Failure.Human gene therapy. Clinical development · 2017Review
- Systemic delivery of adeno-associated viral vectors.Current opinion in virology · 2016Review
- 100-fold but not 50-fold dystrophin overexpression aggravates electrocardiographic defects in the mdx model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2016Article
- Safe and bodywide muscle transduction in young adult Duchenne muscular dystrophy dogs with adeno-associated virus.Human molecular genetics · 2015Article
- Viral vector-mediated gene therapies.Current opinion in neurology · 2015Review
- Contemporary Animal Models For Human Gene Therapy Applications.Current gene therapy · 2015Review
- Prospect of gene therapy for cardiomyopathy in hereditary muscular dystrophy.Expert opinion on orphan drugsArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Adeno-associated virus serotype-8 and 9 (AAV-8 and 9) are the leading candidate vectors to test bodywide neonatal muscle gene therapy in large mammals. We have previously shown that systemic injection of 2-2.5×10(14) viral genome (vg) particles/kg of AAV-9 resulted in widespread skeletal muscle gene transfer in newborn dogs. However, nominal transduction was observed in the heart. In contrast, robust expression was achieved in both skeletal muscle and heart in neonatal dogs with 7.14-9.06×10(14) vg particles/kg of AAV-8. To determine whether superior cardiac transduction of AAV-8 is because of the higher vector dose, we delivered 6.14×10(14) and 9.65×10(14) vg particles/kg of AAV-9 to newborn puppies via the jugular vein. Transduction was examined 2.5 months later. Consistent with our previous reports, we observed robust bodywide transduction in skeletal muscle. However, increased AAV dose only moderately improved heart transduction. It never reached the level achieved by AAV-8. Our results suggest that differential cardiac transduction by AAV-8 and AAV-9 is likely because of the intrinsic property of the viral capsid rather than the vector dose.
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Registered trials
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.