Abstract
with some preliminary data indicating that at least one of the mutations in NS4B confers partial Legalon-SIL resistance in cell culture. Conclusion: Mutations selected during Legalon-SIL treatment in vivo and in cell culture primarily map to viral membrane attachment regions in NS3 and NS4B, arguing for a primary mode of action targeting RNA replication independent of inhibition of the viral polymerase. Further phenotypic analysis of the mutants will help to elucidate the mechanism of action of Silibinin.
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