Recombinant adenovirus vectors are widely used in gene therapy due to their advantages of wide host cell range, large insertable fragments, and high virus titers. However, in practical applications, there are still shortcomings such as low infection efficiency and lack of host targeting. Modifying it can improve the efficiency and targeting of adenovirus infection.

Adenovirus infects cells in two steps: firstly, the knob domain in the viral capsid fiber (fiber) recognizes and binds to the "coxsackie virus and adenovirus receptor" (CAR) on the cell surface, and mediates the interaction of viral particles with adenovirus. cell surface contact. It then recognizes and binds to the integrin ave3 and ave5 receptors through the RGD structure of the coat penton protein. Internalization of viruses through receptor-mediated endocytosis. Due to the low expression of CAR and integrin receptors on the surface of some tumor cells, the efficiency of adenovirus infection of tumor cells is low. therefore . One strategy for transforming adenovirus is to recombine the previous RGD peptide (such as RGD-4C) at the C-terminal of fibrin or the HI loop of the knob domain. Establish a CAR-independent specific infection pathway, thereby improving the targeting of Ad to tumor cells. This RGD-modified recombinant adenoviral vector is able to transfect tumor cells in a CAR-independent manner for some malignant tumors such as osteosarcoma, glioma, ovarian tumor, and pancreatic cancer for which traditional adenoviral gene therapy is unsatisfactory. The transfection efficiency was greatly improved. It provides feasibility for clinical gene therapy of such tumors.

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