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RNA aptamer-mediated interference of HCV replication by targeting the CRE-5BSL3.2 domain.

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  • Author(s): Marton S;Marton S; Romero-López C; Berzal-Herranz A
  • Source:
    Journal of viral hepatitis [J Viral Hepat] 2013 Feb; Vol. 20 (2), pp. 103-12. Date of Electronic Publication: 2012 Jul 17.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Blackwell Scientific Publications Country of Publication: England NLM ID: 9435672 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2893 (Electronic) Linking ISSN: 13520504 NLM ISO Abbreviation: J Viral Hepat Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford ; Boston : Blackwell Scientific Publications, 1994-
    • Subject Terms:
      Virus Replication*; Aptamers, Nucleotide/*genetics ; Hepacivirus/*physiology ; Viral Nonstructural Proteins/*genetics; Base Sequence ; Binding Sites ; Binding, Competitive ; Cell Line, Tumor ; Consensus Sequence ; Hepacivirus/genetics ; Humans ; Inverted Repeat Sequences ; Molecular Sequence Data ; Regulatory Sequences, Ribonucleic Acid ; SELEX Aptamer Technique
    • Abstract:
      The RNA genome of hepatitis C virus (HCV) contains multiple conserved structural RNA domains that play key roles in essential viral processes. A conserved structural component within the 3' end of the region coding for viral RNA-dependent RNA polymerase (NS5B) has been characterized as a functional cis-acting replication element (CRE). This study reports the ability of two RNA aptamers, P-58 and P-78, to interfere with HCV replication by targeting the essential 5BSL3.2 domain within this CRE. Structure-probing assays showed the binding of the aptamers to the CRE results in a structural reorganization of the apical portion of the 5BSL3.2 stem-loop domain. This interfered with the binding of the NS5B protein to the CRE and induced a significant reduction in HCV replication (≈50%) in an autonomous subgenomic HCV replication system. These results highlight the potential of this CRE as a target for the development of anti-HCV therapies and underscore the potential of antiviral agents based on RNA aptamer molecules.
      (© 2012 Blackwell Publishing Ltd.)
    • Accession Number:
      0 (Aptamers, Nucleotide)
      0 (Regulatory Sequences, Ribonucleic Acid)
      0 (Viral Nonstructural Proteins)
      EC 2.7.7.48 (NS-5 protein, hepatitis C virus)
    • Publication Date:
      Date Created: 20130111 Date Completed: 20130613 Latest Revision: 20220110
    • Publication Date:
      20231215
    • Accession Number:
      10.1111/j.1365-2893.2012.01629.x
    • Accession Number:
      23301545