New findings published by UW Medicine and collaborators indicates that a drug-like molecule can activate innate immunity and induce genes to control infection in a range of RNA viruses, including dengue, West Nile, hepatitis C, influenza A, Nipah, Lassa, respiratory syncytial and Ebola. The study was reported last week in the Journal of Virology. It shows promising evidence for creating a broad-spectrum antiviral.
"Our compound has an antiviral effect against all these viruses," said Michael Gale Jr., University of Washington professor of immunology and director of the UW Center for Innate Immunity and Immune Disease.
The findings firstly show that innate immunity can be triggered therapeutically through a molecule present in all our cells, known as RIG-I. RIG-I is a cellular protein which is known as a pathogen recognition receptor. These receptors detect viral RNA and signal an innate immune response inside the cell that is essential for limiting and controlling viral infections. The signal induces the expression of many innate immune and antiviral genes and the production of antiviral gene products, pro-inflammatory cytokines, chemokines and interferons. The researchers noted that these products work together to suppress and control virus infection.
This kind of activation has been tested successfully in cells and in lab mice. What will be aimed at next time would be to test dosing and stability in animal models and subsequently in humans. It is a process that may take 2 to 5 years, according to Gale.
Some viral infections can't be treated by traditional antivirals. Activating innate immunity also will make the viruses less likely to resist the drug actions because the therapy targets the cell via gene action but not the virus itself.
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