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Animal virus replication and RNAi-mediated antiviral silencing in Caenorhabditis elegans
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Animal virus replication and RNAi-mediated antiviral silencing in Caenorhabditis elegans
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Journal Article
Animal virus replication and RNAi-mediated antiviral silencing in Caenorhabditis elegans
2005
Overview
Super model for viruses
The nematode
Caenorhabditis elegans
is an ideal model for the study of many aspects of cell biology, including the hot topic of RNA interference (RNAi). But there was a problem in using the worm to study antiviral RNAi responses:
C. elegans
seemed not to support viral replication. But now the insect pathogen Flock house virus and the mammalian pathogen vesicular stomatitis virus are both shown to infect the worm, and to provoke a strong RNAi-based antiviral defence. So this important genetic model is now available for the study of host–virus interactions, and the antiviral effect of RNAi.
The worm
Caenorhabditis elegans
is a model system for studying many aspects of biology, including host responses to bacterial pathogens
1
,
2
, but it is not known to support replication of any virus. Plants and insects encode multiple Dicer enzymes that recognize distinct precursors of small RNAs and may act cooperatively
3
,
4
,
5
,
6
,
7
. However, it is not known whether the single Dicer of worms and mammals is able to initiate the small RNA-guided RNA interference (RNAi) antiviral immunity as occurs in plants
8
and insects
9
. Here we show complete replication of the Flock house virus (FHV) bipartite, plus-strand RNA genome in
C. elegans
. We show that FHV replication in
C. elegans
triggers potent antiviral silencing that requires RDE-1, an Argonaute protein
10
,
11
essential for RNAi mediated by small interfering RNAs (siRNAs) but not by microRNAs. This immunity system is capable of rapid virus clearance in the absence of FHV B2 protein, which acts as a broad-spectrum RNAi inhibitor
9
,
12
upstream of
rde-1
by targeting the siRNA precursor. This work establishes a
C. elegans
model for genetic studies of animal virus–host interactions and indicates that mammals might use a siRNA pathway as an antiviral response.
Publisher
Nature Publishing Group UK,Nature Publishing,Nature Publishing Group
Subject
/ Animals, Genetically Modified
/ Biological and medical sciences
/ Caenorhabditis elegans - genetics
/ Caenorhabditis elegans - virology
/ Caenorhabditis elegans Proteins - genetics
/ Caenorhabditis elegans Proteins - metabolism
/ Fundamental and applied biological sciences. Psychology
/ Gene Expression Regulation, Viral
/ Genetics
/ Herpesviridae - growth & development
/ Humanities and Social Sciences
/ Insects
/ letter
/ Mammals
/ Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains
/ Ribonuclease III - metabolism
/ RNA
/ RNA, Double-Stranded - genetics
/ RNA, Double-Stranded - metabolism
/ RNA, Small Interfering - genetics
/ RNA, Small Interfering - metabolism
/ Science
/ Virology
/ Virus Replication - genetics
/ Viruses
