Ihmisen RISC koneisto ja virusinfektio (2006 kaavakuva)

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The interplay between virus infection and the cellular RNA interference machinery

Edited by Horst Feldmann

JoostHaasnoot

https://doi.org/10.1016/j.febslet.2006.02.070Get rights and content

Abstract

RNA interference (RNAi) plays a pivotal role in the regulation of gene expression to control cell development and differentiation. In plants, insects and nematodes RNAi also functions as an innate defence response against viruses. Similarly, there is accumulating evidence that RNAi functions as an antiviral defence mechanism in mammalian cells. Viruses have evolved highly sophisticated mechanisms for interacting with the host cell machinery, and recent evidence indicates that this also involves RNAi pathways. The cellular RNAi machinery can inhibit virus replication, but viruses may also exploit the RNAi machinery for their own replication. In addition, viruses can encode proteins or RNA molecules that suppress existing RNAi pathways or trigger the silencing of specific host genes. Besides the natural interplay between RNAi and viruses, induced RNAi provides an attractive therapy approach for the fight against human pathogenic viruses. Here, we summarize the latest news on virus–RNAi interactions and RNAi based antiviral therapy.

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Fig. 1. Viral factors affecting cellular RNAi pathways. miRNA regulated gene expression starts with primiRNAs in the nucleus, which are processed into mature miRNAs by Drosha and Dicer (left panel). The antiviral RNAi response is triggered by virus-derived dsRNAs during infection (right panel). Viral RNAi suppressor factors (proteins or decoy RNAs; middle panel) counter these effects. Viruses can also encode miRNA-like molecules targeting cellular mRNAs. Both RNAi suppressors and viral miRNAs can potentially affect cellular miRNA processing and function (arrows with question mark).