GFP Adeno-Associated Virus ( AAV-VNT )

The vascular endothelium plays a key role in vascular homeostasis and regulation of vascular tone. Endothelial dysfunction is at the root of a variety of diseases that affect the cardiovascular system, such as atherosclerosis, hypertension, and ischemic arterial disease. Therefore, the endothelium is an attractive therapeutic target for both pharmacological and genetic interventions. The ability to specifically target the vasculature in selected organs via the systemic circulation would have important clinical implications. Modification of viral capsids to incorporate cell selectivity has emerged as an avenue for creating “designer” viral vectors for specific applications. In this regard, AAV vectors are attractive for in vivo vascular gene therapy. Unfortunately, they have a poor natural tropism for endothelial cells (ECs). GFP adeno-associated virus (AAV-VNT) represents a major advancement in the field of viral vectors. This particular virus is a reporter gene AAV that has been precisely capsid engineered and modified to enhance its functionality and specificity. AAV-VNT is derived from serotype 2 of the adeno-associated virus (AAV2). AAV2 is known for its versatility and efficiency in transducing a variety of cell types, making it a popular choice for gene delivery systems. Specific insertion of the peptide sequence VNTANST at the I587 site of the AAV2 capsid can enhance the ability of the virus to selectively target and transduce endothelial cells.