RETRACTED ARTICLE: Small interfering RNA targeted to stem-loop II of the 5' untranslated region effectively inhibits expression of six HCV genotypes

Prabhu, Ramesh; Garry, Robert F.; Dash, Srikanta

doi:10.1186/1743-422x-3-100

Cited by 42 publications

(15 citation statements)

References 41 publications

(39 reference statements)

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“…[143] Design of catalytic metallodrugs that perform RNA cleavaget owardsS LIIb can potentially inhibitthe expression of viral proteins. [144] To design ac atalytic metallodrug that targetsS LIIb of IRES RNA, at etrapeptide YrFK that selectively binds to SLIIb was used to bring the catalytic domain (CuGGH) into close proximity with the RNA substrate. [32] The designed catalytic metallodrug, CuGGHYrFK induces selectiveR NA cleavaget owards am odel oligonucleotide derived from SLIIb( 5 '-fluorescein-GGCAGAAAGCGU-CUAGCCAUGGCGUUAGUA UGCC-3').…”

Section: Rna-targeting Catalyticmetallodrugsmentioning

confidence: 99%

Catalytic Metallodrugs: Substrate‐Selective Metal Catalysts as Therapeutics

Cowan

2017

Chemistry A European J

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Metal complexes that catalyze inactivation and degradation of biomolecular targets can be developed into novel therapeutics (catalytic metallodrugs) against a variety of diseases. Despite recent advances in the field, a lack of substrate selectivity is a major hindrance to the development of catalytic metallodrugs for application in clinical practice. Improved targeting can minimize nonselective activity and the potential for side effects. Herein, we focus on recent developments toward novel metal catalysts that exhibit substrate selectivity against a variety of therapeutically relevant biomolecules. Design strategies for developing selective catalytic metallodrugs are also highlighted.

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Section: Rna-targeting Catalyticmetallodrugsmentioning

confidence: 99%

Catalytic Metallodrugs: Substrate‐Selective Metal Catalysts as Therapeutics

Cowan

2017

Chemistry A European J

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“…The other two (5’ UTR and NS5A) molecules only moderately knocked down the virus (< 70%). Although some studies have found that virus replication may be reduced using siRNAs directed to the 5’UTR [ 34 , 35 ] or NS5A [ 16 , 36 ], our DsiRNA molecules targeting those regions were not very efficient. Specifically, the low efficiency of the 5’UTR-targeted sequence is likely due to the highly structured nature of this site [ 37 ], which may hinder the binding of the DsiRNA molecule to its target sequence.…”

Section: Discussionmentioning

confidence: 73%

Evaluation of Canonical siRNA and Dicer Substrate RNA for Inhibition of Hepatitis C Virus Genome Replication – A Comparative Study

et al. 2015

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Hepatitis C virus (HCV) frequently establishes persistent infections in the liver, leading to the development of chronic hepatitis and, potentially, to liver cirrhosis and hepatocellular carcinoma at later stages. The objective of this study was to test the ability of five Dicer substrate siRNAs (DsiRNA) to inhibit HCV replication and to compare these molecules to canonical 21 nt siRNA. DsiRNA molecules were designed to target five distinct regions of the HCV genome – the 5’ UTR and the coding regions for NS3, NS4B, NS5A or NS5B. These molecules were transfected into Huh7.5 cells that stably harboured an HCV subgenomic replicon expressing a firefly luciferase/neoR reporter (SGR-Feo-JFH-1) and were also tested on HCVcc-infected cells. All of the DsiRNAs inhibited HCV replication in both the subgenomic system and HCVcc-infected cells. When DsiRNAs were transfected prior to infection with HCVcc, the inhibition levels reached 99.5%. When directly compared, canonical siRNA and DsiRNA exhibited similar potency of virus inhibition. Furthermore, both types of molecules exhibited similar dynamics of inhibition and frequencies of resistant mutants after 21 days of treatment. Thus, DsiRNA molecules are as potent as 21 nt siRNAs for the inhibition of HCV replication and may provide future approaches for HCV therapy if the emergence of resistant mutants can be addressed.

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“…These reports demonstrated that siRNA targeting the HCV 5'-UTR resulted in 80%-90% inhibition of HCV. Prabhu et al [96] showed that siRNA that targets the highly conserved stem loop Ⅱ region of the HCV IRES efficiently inhibited translation and replication of infectious full-length clones of HCV 1a and 1b strains. Moreover, this siRNA effectively mediated degradation of the HCV IRES RNA and inhibited GFP expression that was controlled by the IRES sequences of six different HCV genotypes.…”

Section: Rnai Against Hcv 5'-and 3'-utr Sequencesmentioning

confidence: 99%

“…Target RNA cleavage or translation inhibition 5'-UTR and 3'-UTR [93][94][95][96][100][101][102] Protein coding regions [103][104][105][106][107][108][109] Antisense oligonucleotide Bind to complementary RNAs and suppress the access to cellular machinery, thereby inhibiting expression or function of the targeted RNAs 5'-UTR [134][135][136][137] Completion of Phase Ⅱ…”

Section: Rnaimentioning

confidence: 99%

Prospects for nucleic acid-based therapeutics against hepatitis C virus

Lee

Kim

Lee

2013

WJG

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In this review, we discuss recent advances in nucleic acid-based therapeutic technologies that target hepatitis C virus (HCV) infection. Because the HCV genome is present exclusively in RNA form during replication, various nucleic acid-based therapeutic approaches targeting the HCV genome, such as ribozymes, aptamers, siRNAs, and antisense oligonucleotides, have been suggested as potential tools against HCV. Nucleic acids are potentially immunogenic and typically require a delivery tool to be utilized as therapeutics. These limitations have hampered the clinical development of nucleic acid-based therapeutics. However, despite these limitations, nucleic acid-based therapeutics has clinical value due to their great specificity, easy and large-scale synthesis with chemical methods, and pharmaceutical flexibility. Moreover, nucleic acid therapeutics are expected to broaden the range of targetable molecules essential for the HCV replication cycle, and therefore they may prove to be more effective than existing therapeutics, such as interferon-α and ribavirin combination therapy. This review focuses on the current status and future prospects of ribozymes, aptamers, siRNAs, and antisense oligonucleotides as therapeutic reagents against HCV.

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RETRACTED ARTICLE: Small interfering RNA targeted to stem-loop II of the 5' untranslated region effectively inhibits expression of six HCV genotypes

Cited by 42 publications

References 41 publications

Catalytic Metallodrugs: Substrate‐Selective Metal Catalysts as Therapeutics

Catalytic Metallodrugs: Substrate‐Selective Metal Catalysts as Therapeutics

Evaluation of Canonical siRNA and Dicer Substrate RNA for Inhibition of Hepatitis C Virus Genome Replication – A Comparative Study

Prospects for nucleic acid-based therapeutics against hepatitis C virus

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