The Hepatitis C Virus contains a noncoding region known as an internal ribosome entry site (IRES) attached upstream of the coding region of the RNA. This site allows for the virus to undergo cap-independent translation of viral RNA, removing the need for many host initiation factors. Our lab has found that a highly conserved loop segment of this IRES RNA plays an essential role in the IRES-driven translation initiation. Previous studies in our lab have found that this IRES domain can be bound by guanine, and that this binding changes the conformation of the internal loop. I have synthesized multiple benzene-fused heterocycles, designed around the hydrogen bonding profile of guanine. Many of these heterocycles contain scaffolds already common in approved drugs. Through a FRET based screening method used by the Hermann lab we can determine the binding affinities of these compounds to the target RNA loop. The compounds with strong enough affinities will then be tested through in vivo models.

Small molecule synthesis of potential inhibitors of hepatitis C virus translation

251st National Meeting (2016)

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