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Beatriz Berzal-Herranz
Researcher at Spanish National Research Council
Publications - 8
Citations - 91
Beatriz Berzal-Herranz is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: RNA & Viral replication. The author has an hindex of 6, co-authored 8 publications receiving 79 citations.
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An engineered inhibitor RNA that efficiently interferes with hepatitis C virus translation and replication.
TL;DR: The present work analyses the anti-HCV potential of HH363-24, an in vitro selected molecule composed of a catalytic RNA cleaving domain with an extension at the 3' end that acts as aptamer for the viral 5'UTR.
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Silencing of hepatitis C virus replication by a non-viral vector based on solid lipid nanoparticles containing a shRNA targeted to the internal ribosome entry site (IRES)
Josune Torrecilla,Ana del Pozo-Rodríguez,María ÿngeles Solinís,P. S. Apaolaza,Beatriz Berzal-Herranz,Cristina Romero-López,Alfredo Berzal-Herranz,Alicia Rodríguez-Gascón +7 more
TL;DR: A non-viral vector based on solid lipid nanoparticles bearing hyaluronic acid, protamine and a short hairpin RNA targeted to the Internal Ribosome Entry Site (IRES) of the HCV is shown for the first time to silence a HCV replicon.
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Anti-HCV RNA Aptamers Targeting the Genomic cis-Acting Replication Element
Soledad Marton,Beatriz Berzal-Herranz,Eva Garmendia,Francisco J. Cueto,Alfredo Berzal-Herranz +4 more
TL;DR: Inhibition assays showed that the selected RNAs significantly inhibit the replication of a subgenomic HCV replicon in Huh-7 cell cultures, highlighting the potential of aptamer RNA molecules as therapeutic antiviral agents.
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Development of Optimized Inhibitor RNAs Allowing Multisite-Targeting of the HCV Genome
TL;DR: The feasibility of using in vitro selection strategies for obtaining improved RNA molecules with potential clinical applications is highlighted, including the anti-HCV chimeric inhibitor RNA HH363-10, which has a hammerhead catalytic domain and an aptamer RNA domain.
Journal ArticleDOI
The HCV genome domains 5BSL3.1 and 5BSL3.3 act as managers of translation
TL;DR: The present data show that the CRE promotes a defect in polysome production, and hinders the assembly of the 80S complex, likely through the direct, high affinity recruitment of the 40S ribosomal subunit, which supports a model in which the CRE-mediated inhibition of viral translation is a multifactorial process defined by the establishment of long-range RNA-RNA interactions.