Hexon-Modified Adenovirus Vectors that are Unable to Bind Human Blood Factors and their Use

Introduction Human species C adenovirus serotype 5 (Ad5) is the most common viral vector used in clinical studies worldwide. Ad5 vectors infect liver cells in vivo with high efficiency via a poorly defined mechanism, which involves virus binding to vitamin K-dependent blood coagulation factors. The efficient interaction between Ad5 and liver cells, which sequester a large proportion of the delivered vector dose, represents a significant hindrance if gene delivery to extrahepatic cells and tissues is required. The development of adenovirus not interacting with liver cells would not only increase extrahepatic delivery but also decrease adenovirus-associated toxicity. Technology description Dr Shayakhmetov and collaborators have recently demonstrated the critical role of the major Ad5 capsid protein hexon, for virus infection of hepatocytes in vivo. Hexon-mutated virus bearing a large insertion in hexon show markedly reduced FX binding in vitro and fail to deliver a transgene to hepatocytes in vivo. This invention includes compositions and methods aimed at reducing toxicity associated with adenovirus administrations, by mutating hexon proteins in various locations. Business Opportunity This invention has important practical implications for development of safe and efficient cell- and tissue-type-specific adenovirus vectors for gene therapy applications. Intellectual Property Position The University of Washington has applied to patent protection to secure the rights to this technology. Related Publication(s)
Proc Natl Acad Sci U S A. 2008 Apr 8;105(14):5483-8 For more information on this technology contact:
Valerie Carricaburu, Ph.D. Technology Manager UW TechTransfer, Invention Licensing [email protected] 206-543-3970

Type of Offer: Licensing



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