Key result
Aptamers targeting RNA hairpins selectively inhibited in vitro TAR-dependent transcription of HIV-1 and specifically blocked translation of HCV in cell-free assays and cultured cells.
Aptamers targeting specific viral RNA hairpins can effectively inhibit HIV-1 transcription and HCV translation in preclinical models.
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Preclinical aptamer activity in HIV-1 and HCV models leaves open clinical translation pending in vivo efficacy and safety data.
Oligonucleotides exhibiting a strong affinity and a high specificity for RNA hairpins were obtained by in vitro selection. Such oligomers give rise to loop-loop complexes with the target hairpins: the trans-activation responsive (TAR) element of the Human Immunodeficiency virus-1 (HIV-1) or subdomains of the Hepatitis C virus (HCV) mRNA. Chemically modified derivatives of an antiTAR aptamer were shown to compete out the binding of the viral protein Tat and to selectively inhibit the in vitro TAR-dependent transcription of a reporter gene. In addition, antisense oligomers derived from sequences selected against the domain IIId of the HCV internal ribosome entry site were shown to specifically block translation both in a cell-free assay and in cultured cells.
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Toulmé et al. (2003) studied HIV-1 and HCV infection (in vitro models). Aptamers to RNA structures (antiTAR aptamer and antisense oligomers) was evaluated on Inhibition of TAR-dependent transcription and translation. Aptamers targeting RNA hairpins selectively inhibited in vitro TAR-dependent transcription of HIV-1 and specifically blocked translation of HCV in cell-free assays and cultured cells.
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