Hepatitis C virus (HCV), a positive-sense RNA virus that chronically infects between 2.7 and 3.9 million Americans, is highly mutational, making the HCV infection difficult to treat. Thus, it is of high interest to search for highly conserved therapeutic targets within the HCV genome. Two such sequences are located within the 5' untranslated region (UTR) of HCV, being complementary for the microRNA miR-122, a liver microRNA essential for the production of the infectious virus. The use of peptide nucleic acids (PNAs) as therapeutic agents has become a promising area of study in recent years. In this study, we characterized the interactions between miR-122 and the HCV 5'UTR and designed PNAs to disrupt these interactions and thus, inhibit RNA replication and translation. Our results show that the PNAs effectively disrupt the interactions involving miR-122 and the 5'UTR, thereby increasing the possibility of a new therapeutic option against HCV. / Bayer School of Natural and Environmental Sciences / Chemistry and Biochemistry / MS / Thesis