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Experimental RNAi02:15

Experimental RNAi

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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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RNA Interference01:23

RNA Interference

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RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...
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siRNA - Small Interfering RNAs02:30

siRNA - Small Interfering RNAs

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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
In the cytoplasm, siRNA is processed from a double-stranded RNA, which comes from either endogenous DNA transcription or exogenous sources like a virus. This double-stranded RNA is then cleaved by the...
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Regulation of the Unfolded Protein Response01:31

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Related Experiment Video

Updated: Jun 11, 2025

High-throughput Screening for Broad-spectrum Chemical Inhibitors of RNA Viruses
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High-throughput Screening for Broad-spectrum Chemical Inhibitors of RNA Viruses

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Combining RNA Interference and RIG-I Activation to Inhibit Hepatitis E Virus Replication.

Mathias Ziersch1, Dominik Harms2, Lena Neumair1

  • 1Applied Biochemistry, Institute of Biotechnology, Technische Universität Berlin, 13355 Berlin, Germany.

Viruses
|September 28, 2024
PubMed
Summary

Hepatitis E virus (HEV) RNA interference (RNAi) therapies show promise. Small interfering RNAs (siRNAs) targeting conserved HEV regions and activating RIG-I effectively inhibit viral replication, offering new therapeutic avenues.

Keywords:
HEVRIG-IRNA 5′triphosphateRNAi therapysiRNA

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Related Experiment Videos

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Area of Science:

  • Virology
  • Immunology
  • RNA Therapeutics

Background:

  • Hepatitis E virus (HEV) causes significant global health issues, with limited treatment options.
  • Severe outcomes are common in pregnant women and those with liver disease.
  • RNA interference (RNAi) presents a potential targeted therapeutic strategy.

Purpose of the Study:

  • To design and evaluate small interfering RNAs (siRNAs) for Hepatitis E virus (HEV) inhibition.
  • To investigate the efficacy of siRNAs targeting conserved HEV genomic regions.
  • To explore the role of siRNA modifications in activating innate immune responses.

Main Methods:

  • Designed siRNAs targeting HEV helicase and ORF3 conserved regions.
  • Tested siRNA efficacy in HEV-infected A549 cells and a persistent infection model.
  • Assessed the impact of 5' triphosphate modification on siRNA-mediated RIG-I activation.

Main Results:

  • siRNAs targeting ORF3 significantly inhibited HEV replication in infected cells.
  • Effective inhibition was observed in a cell line modeling chronic HEV infection.
  • 5' triphosphate modification activated RIG-I, enhancing HEV replication suppression.

Conclusions:

  • siRNAs targeting conserved HEV regions are effective against viral replication.
  • A dual-action strategy combining RNAi and RIG-I activation shows therapeutic potential.
  • This approach may lead to novel treatments for Hepatitis E.