Journal
NATURE CHEMICAL BIOLOGY
Volume 5, Issue 11, Pages 823-825Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nchembio.217
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Funding
- NIAID NIH HHS [K08 AI069989, R01 AI072012, K08 AI069989-02, R01AI72012] Funding Source: Medline
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The internal ribosome entry site (IRES), a highly conserved structured element of the hepatitis C virus (HCV) genomic RNA, is an attractive target for antiviral drugs. Here we show that benzimidazole inhibitors of the HCV replicon act by conformational induction of a widened interhelical angle in the IRES subdomain IIa, which facilitates the undocking of subdomain IIb from the ribosome and ultimately leads to inhibition of IRES-driven translation in HCV-infected cells.
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