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RACING to HALT the Zika virus in its spread around the world
EVERY COUPLE OF WEEKS, an eagerly awaited package arrives at a University of Washington research lab in South Lake Union. Inside, nestled in dry ice, are special chemical compounds that Dr. Michael Gale Jr. affectionately dubs his “favorite molecules.” These “small molecules” have the potential to stop the Zika virus in its tracks. At the UW’s Center for Innate Immunity & Immune Disease, Gale, ’85, ’94, who is the director, is on the hunt for the right one to constitute a drug to sideline the mosquito-borne illness that has dominated headlines this year, as well as other related viruses. His ace in the hole may be RIG-I, aka retinoic acid-inducible gene I, which was identified in 2005 when he was an assistant professor at the University of Texas Southwestern Medical Center in Dallas. The discovery emerged as Gale and his colleagues were trying to discern how the body triggers an immune response to hepatitis C. RIG-I, they realized, functioned as an “on-off switch” for immunity against the virus. Over a period of years, the researchers figured out that RIG-I kicks into gear when it recognizes and binds to viral RNA, triggering the immune response. Hepatitis C and Zika virus are both RNA viruses (viruses with an RNA genome, as opposed to DNA viruses); so are West Nile, which like the Zika virus infects the brain, and Ebola, which causes deadly hemorrhagic fever—not to mention the common cold and influenza viruses. Gale and the 34 researchers in his lab, in collaboration with Kineta, a local biotech company in which Gale is a founding scientist, are now in the process of testing various small molecules—organic compounds that are tiny enough to infiltrate cells and comprise most drugs—to nail the right formulation to attack these RNA viruses. They’ve screened thousands of molecules to identify a few that activate RIG-I and subsequently induce an immune response that stops the viruses.
Full Article: "Zeroing in on Zika" By Bonnie Rochman