Mouse Model of Individual Unresponsive to Interferon
NIAID has developed a mouse model that produces very high levels of Interferon-alpha-receptor 2 (IFNAR2), both in liver cells and free-floating in serum.
Chronic co-infection of HIV and hepatitis C virus (HCV) is associated with increased overall morbidity and mortality compared to those infected with just one virus. Recent data further suggests that co-infection is also associated with a more rapid progression of liver disease, higher HCV RNA viral levels, decreased cure rate of HCV, and increased toxicities of anti-HCV therapy. Finally, clinical trials have shown that many patients infected with both viruses do not respond to Interferon-based therapy. Research strongly suggests that non-responding patients have an increased level of a free-floating form of IFNAR2, which could block Interferon activity.
Resistance to Interferon therapy also occurs in other diseases, such as autoimmune diseases (e.g., lupus, scleroderma, psoriasis, vasculitis) and certain forms of cancer (e.g., Kaposi’s sarcoma, follicular lymphoma). The various means by which resistance arises is currently being researched.
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Shyamasundaran Kottilil (NIAID)
Howard Young (NCI)
Michael Polis (NIAID)
Anthony Suffredini (CC)
Research Tool -- patent protection is not being pursued for this technology
The National Institute of Allergy and Infectious Diseases, Laboratory of Immunoregulation, is interested in collaborative research directed toward molecular strategies for vaccine and antiviral development, and animal models of viral hepatitis C. Please contact William Ronnenberg at 301-451-3522 or email@example.com for more information.
Susan Ano , Ph.D.
NIH Office of Technology Transfer
OTT Reference No: E-106-2009/0