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RNA Interference

RNA Interference

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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Related Experiment Video

Updated: Nov 6, 2025

Rescue of Recombinant Newcastle Disease Virus from cDNA

Rescue of Recombinant Newcastle Disease Virus from cDNA

Published on: October 11, 2013

Interferon antagonism by SARS-CoV-2: a functional study using reverse genetics.

Simon Schroeder¹, Fabian Pott^1,2, Daniela Niemeyer¹

¹Institute of Virology, Charité-Universitätsmedizin Berlin, Berlin, Germany.

The Lancet. Microbe

|May 10, 2021

Summary

SARS-CoV-2 ORF6 shows weaker interferon antagonism than SARS-CoV ORF6, impacting viral fitness. Monitoring specific amino acid changes in ORF6 is crucial for understanding viral adaptation and potential pandemic threats.

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Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2

Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2

Published on: November 5, 2021

Area of Science:

Virology
Immunology
Molecular Biology

Background:

SARS-CoV-2 and SARS-CoV share homologous proteins and entry receptors but differ in transmission and pathogenesis.
Understanding these differences is key to controlling COVID-19 and future coronavirus outbreaks.

Purpose of the Study:

To compare the interferon antagonism capabilities of SARS-CoV and SARS-CoV-2.
To investigate the role of ORF6 protein in differential interferon signaling interference.

Main Methods:

Infection of Vero E6 and Calu-3 cells with SARS-CoV and SARS-CoV-2.
Analysis of viral replication, TMPRSS2-dependent entry, and sensitivity to type I interferon.
Assessment of cytokine induction and interferon signaling pathways.
Reverse genetic engineering of SARS-CoV ORF6 to study its role in interferon antagonism.

Main Results:

SARS-CoV replicated more efficiently in Vero E6 cells, while SARS-CoV-2 replicated better in Calu-3 cells, linked to TMPRSS2 expression.
SARS-CoV-2 was more sensitive to interferon and less efficient at suppressing IRF3 nuclear translocation and interferon-stimulated gene induction compared to SARS-CoV.
SARS-CoV-2 ORF6 exhibited weaker antagonism of interferon signaling than SARS-CoV ORF6, with specific amino acid substitutions influencing this activity.

Conclusions:

SARS-CoV-2 ORF6 demonstrates reduced interference with human interferon induction and signaling compared to SARS-CoV ORF6.
Functional optimization of interferon antagonism via changes in ORF6, particularly at positions 51 and 56, may be selected for viral fitness.
Monitoring these specific amino acid residues in ORF6 is recommended for assessing potential adaptive changes in SARS-CoV-2.