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Credit: Mary Ann Liebert, Inc., publishers
New Rochelle, NY, January 15, 2021 The biodistribution of adeno-associated virus (AAV) gene transfer vectors can be measured in nonhuman primates using a new method. The method quantifies whole-body and organ-specific AAV capsids from 1 to 72 hours after administration. Study design and results are presented in the peer-reviewed journal
Human Gene Therapy. Click here to read the full-text article free on the
Human Gene Therapy website through February 15, 2021.
AAV capsids were labeled with I-124 and delivered using two routes of administration: intravenous and directly into the cerebrospinal fluid (CSF). Biodistribution was measured by quantitative positron emission tomography (PET) at 1, 24, 48, and 72 hours after AAV administration. Two AAV vectors - AAVrsh.10 and AAV9 - we
4.1 Recent Developments - Importance and How to Use This Section
4.1.1 Importance of These Developments
4.1.2 How to Use This Section
Genetron Health Targeting Early Cancer Detection
Pan-European Initiative to Build Tools for Sharing Genomic Data
UK Government Unveils New Genomic Healthcare Strategy
Foundation Medicine Liquid Biopsy Gets FDA Approval
American Heart Association Develops Genetic Testing Guidelines
Yourgene Health Gets CE Mark for Iona NIPT Test
NorthShore Looks to Expand Genomics Integration Into Primary Care
Germline Results From Tumor-Normal Sequencing Guides Precision Therapy in Advanced Cancer Patients
FDA Clears Cancer Genomic Profiling Kit From Personal Genome Diagnostics
BillionToOne Closes $15M Series A Follow-on Round
AAV Capsid-Promoter Interaction Shown to Occur in Non-human Primate Brain
December 11, 2020
The phenomenon of adeno-associated virus (AAV) capsid-promoter interaction recently seen in the rat central nervous system has now been shown to occur in the non-human primate brain. This interaction can directly determine cell-specific transgene expression, as described in the article, “Adeno-Associated Virus Capsid-Promoter Interactions in the Brain Translate from Rat to the Nonhuman Primate,” published in
Human Gene Therapy.
An AAV contains a single-stranded DNA genome encapsulated in a capsid comprised of three structural proteins.
“Recently, we established an AAV9 capsid-promoter interaction that directly determined cell-specific gene expression across two synthetic promoters, Cbh and CBA, in the rat striatum. These studies not only expand this capsid-promoter interaction to include another promoter in the rat striatum but also establish AAV capsid-promoter interactions in the
Researchers identify adenovirus gene therapy for placental insufficiency
A new study identified an adenovirus gene therapy vector carrying a VEGF isoform. It can improve uterine blood flow in placental insufficiency, as reported in the peer-reviewed journal
Human Gene Therapy.
Reduced uterine blood flow and lack of bioavailable VEGF due to placental insufficiency is a major cause of severe fetal growth restriction (FGR). This is untreatable and causes serious neonatal morbidity and death.
Anna David, UCL Institute for Women s Health, and colleagues tested different VEGF isoforms on endothelial cells from four species, including from human umbilical vein. The results support the use of the best performing VEGF isoform in a human clinical trial for FGR caused by placental insufficiency.
E-Mail
IMAGE: journal in the field and provides all-inclusive access to the critical pillars of human gene therapy: research, methods, and clinical applications. view more
Credit: Mary Ann Liebert, Inc., publishers
New Rochelle, NY, December 15, 2020 A new study identified an adenovirus gene therapy vector carrying a VEGF isoform. It can improve uterine blood flow in placental insufficiency, as reported in the peer-reviewed journal
Human Gene Therapy. Click here to read the full-text article free on the
Human Gene Therapy website through January 15, 2021.
Reduced uterine blood flow and lack of bioavailable VEGF due to placental insufficiency is a major cause of severe fetal growth restriction (FGR). This is untreatable and causes serious neonatal morbidity and death.