Cellular Receptor for Varicella-Zoster Virus, Methods of Inhibiting Spread of Varicella-Zoster and Methods of Increasing Stability and Infectivity of the Virus
Description of Invention:
This technology relates to identification of insulin degrading enzyme (IDE) as a cellular receptor for Varicella-Zoster-Virus (VZV), the etiologic agent of varicella (chickenpox) and zoster (shingles). Acute infection of VZV is followed by cell-associated viremia and the development of varicella rash. The virus establishes life-long latency in the nervous system and can reactivate to cause zoster. The mechanism of VZV entry into target cells and spread from cell-to-cell is not well understood. The inventors have shown that antibodies to IDE and soluble IDE partially inhibit infection with the virus in cell culture. Reducing the level of IDE in the cell (with siRNA), or blocking the ability of IDE to bind with a VZV glycoprotein, markedly diminishes cell-to-cell spread of the virus in cell culture and partially inhibits infection of cells with cell-free virus. This invention further describes molecules that may have a role in the treatment or prevention of VZV infections, including antibodies to IDE, peptides that block IDE-VZV interactions, and other molecules that block binding activity of IDE.
Applications:
Treatment and prevention of varicella zoster virus infection
Market:
Prophylactics and therapeutics for chickenpox and shingles
For Additional Information Please Contact: Kevin Chang Ph.D.
NIH Office of Technology Transfer
6011 Executive Blvd, Suite 325
Rockville, MD 20852-3804
Phone: 301/435-5018
Email: changke@mail.nih.gov
Fax: 301/402-0220
