Abstract
Background/Aims: Persistent infection with hepatitis C virus (HCV) leads to the development of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. SiRNAs are currently being evaluated as promising therapeutic agents for HCV infection. Unfortunately, the antiviral efficacy of HCV directed siRNAs is limited by emergence of escape variants that are resistant to siRNA because of the high mutation rate of HCV. Alternatively, cellular RNA binding proteins that play an important role in the replication cycle of hepatitis C virus could be more attractive targets for siRNAs to sustain antiviral effects. We have previously shown that PTB-directed siRNAs inhibited subgenomic HCV IRES-mediated translation by depletion of PTB (Polypyrimidine tract binding protein), while PSMA7 (proteasome alpha-subunit 7) and HuR (Human antigen R) directed siRNAs decreased both, HCV replication and translation. In this study we investigated whether the inhibitory effect on subgenomic HCV replication and translation by HCV cofactor directed siRNAs could be significantly increased by synergistic or additive effects of siRNA combinations.
Published Version
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