GFP Adeno-Associated Virus ( AAV-NDVWN )

Different strategies have been developed to achieve higher transduction efficiency and specificity, mainly by modifying the AAV capsid, eliminating natural tropism and repositioning the vector to specific target cell receptors. Vector repositioning can not only improve gene transfer efficiency and reduce adverse side effects, but also minimize immune responses to the vector and the encoded transgene, which is particularly useful for systemic vector applications. Improvements in gene transfer efficiency and specificity can be achieved through rational vector targeting, such as through bispecific adapter molecules or chemical modifications of the AAV capsid. However, such vector modifications are often associated with reduced titers, reduced vector stability, or additional immunogenicity caused by these conjugates. Direct targeting approaches, such as genetic modification of the viral capsid by incorporation of targeting ligands, can circumvent these issues but are always limited to the use of known, defined targeting peptides. GFP AAV-NDVWN particles are derived from AAV serotype 2 (AAV2), which is widely acclaimed by the scientific community for its efficient transduction capacity and relatively low immunogenic response. AAV-NDVWN is unique in its engineered capsid, which includes the insertion of a specific peptide sequence, NDVWNRDNSSKRGGTTEAS, at position I588. This modification is critical because it confers enhanced specificity to the virus for endothelial cells, an important cell type that lines the inner surface of blood vessels. Endothelial cells play a crucial role in a variety of physiological processes, including vascular development, hemostasis, and blood pressure regulation, as well as in pathological conditions such as inflammation, thrombosis, and tumor metastasis. The ability to specifically target these cells with GFP AAV-NDVWN allows researchers to monitor gene expression and cell behavior in real time through green fluorescent protein tagging.