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Basic Characteristics of Mutations
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Mutation Site
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Y93H |
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Mutation Site Sentence
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A mutant form of NS5A (Y93H) that confers resistance to ledipasvir shows diminished binding to ledipasvir. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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NS5A |
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Standardized Encoding Gene
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NS5A
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Genotype/Subtype
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- |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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HCV Infection
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Immune
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- |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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Ledipasvir (LDV) |
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Location
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- |
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Literature Information
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PMID
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25856426
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Title
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Direct binding of ledipasvir to HCV NS5A: mechanism of resistance to an HCV antiviral agent
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Author
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Kwon HJ,Xing W,Chan K,Niedziela-Majka A,Brendza KM,Kirschberg T,Kato D,Link JO,Cheng G,Liu X,Sakowicz R
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Journal
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PloS one
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Journal Info
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2015 Apr 9;10(4):e0122844
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Abstract
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Ledipasvir, a direct acting antiviral agent (DAA) targeting the Hepatitis C Virus NS5A protein, exhibits picomolar activity in replicon cells. While its mechanism of action is unclear, mutations that confer resistance to ledipasvir in HCV replicon cells are located in NS5A, suggesting that NS5A is the direct target of ledipasvir. To date co-precipitation and cross-linking experiments in replicon or NS5A transfected cells have not conclusively shown a direct, specific interaction between NS5A and ledipasvir. Using recombinant, full length NS5A, we show that ledipasvir binds directly, with high affinity and specificity, to NS5A. Ledipasvir binding to recombinant NS5A is saturable with a dissociation constant in the low nanomolar range. A mutant form of NS5A (Y93H) that confers resistance to ledipasvir shows diminished binding to ledipasvir. The current study shows that ledipasvir inhibits NS5A through direct binding and that resistance to ledipasvir is the result of a reduction in binding affinity to NS5A mutants.
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Sequence Data
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-
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